lroot on August 24th, 2018

people socializing

Having a great circle of friends and maintaining strong social networks may just be another key to helping maintain memory and brain health. A study by Ohio State University has discovered that mice which have been housed in groups had much healthier brains and better memories than those who lived in pairs.

The study helps confirm the role social connections make in improving quality of life and preserving memory. Maintaining a large social network can have very positive influences on the aging of the brain says Elizabeth Kirby, assistant professor of behavioral neuroscience and a member of the Center for Chronic Brain Injury at the university. It has already been established that humans have a strong correlation between social connections and cognitive health. What wasn’t clear was whether having a group of friends protected people or if people with brain health that was declining were withdrawing from their connections.

The study was designed to answer this question by using an animal model. Some mice were housed for three months with six roommates to allow for complex interactions. Other mice lived in pairs known as the old couple model. All mice were 15 to 18 months old for the experiment which is a time of natural memory decline in the lifespan of rodents.

When the mice that were group housed were tested for memory they fared much better than the pairs. Moving an object was the test. The group housed mice were better at remembering what they had seen and went to the object in the new location. The paired mice had no idea the object had even been moved.

The researchers also conducted a maze-based memory test with holes that led to escape hatches. The group housed mice improved with each trial memorizing where the escape doors were and walked directly to them. The coupled mice did not get faster even when the tests were repeated several times over the course of a day. They continued to search each hole rather than remembering where the ones were that led to the escape hatch. The group housed mice were using the hippocampus, the area of the brain that relates to good memory function. With age the hippocampus declines fairly markedly even when dementia is not present. Social ties and exercise are known to help improve memory in this part of the brain.

The study indicated the differences appeared to be due to socialization alone as opposed to previous studies which focused on mice that had highly enriched environments comparing them with mice that did not. Further research is planned which will explore the molecular explanations for the connection between improved memory and brain health and socialization. However, the recent study stresses how important social connections are as we age.

To view the original scientific study click here: A Larger Social Network Enhances Novel Object Location Memory and Reduces Hippocampal Microgliosis in Aged Mice. Frontiers in Aging Neuroscience, 2018; 10 DOI: 10.3389/fnagi.2018.00142

lroot on August 17th, 2018

woman in sun

The Journal of the American Osteopathic Association has recently reported a study that discovered nearly 1 billion people around the world are most likely deficient or insufficient in Vitamin D. It is believed that part of the lack of Vitamin D may be due to minimal exposure to the sun by the over use of sunscreen. Chronic Disease is also playing a role in this vitamin deficiency.

Overall people are spending less time outdoors, however when they are they are using large amounts of sunscreen. Sunscreen mitigates the ability of the body to produce Vitamin D and should be used strategically. Some exposure to the sun is necessary for the body to catalyze Vitamin D. People need to be vigilant about protecting themselves against skin cancer, however there are healthy, moderate levels of unprotected sun exposure which is very helpful in boosting Vitamin D.

According to the Endocrine Society, Vitamin Deficiency is realized when levels are below 20mg/ml and insufficiency is realized when levels are between 21 and 30 mg/ml. You can have your level checked with a blood test that your doctor can order.

Vitamin D is also inhibited with a variety of diseases which reduce the body’s ability to metabolize Vitamin D from food. Vitamin D is considered to be a hormone and is generated when skin is subjected to sunlight. Almost every cell in the body has Vitamin D receptors which is why this vitamin plays such a vital role in the body’s functions. From immune system functionality to minimization of inflammation to cell growth modulation and more, Vitamin D is a vital vitamin. Anyone who is Vitamin D deficient or insufficient is prone to bone fractures and weakness of muscles.

The amount of time a person should spend in the sun depends on that person’s idiosyncratic skin pigmentation and geographic location. Lighter skin will synthesize larger amounts of Vitamin D than darker skin. The study discovered that 95% of African American adults might have deficiency or insufficiency of Vitamin D. Variations across races are because of unique levels of skin pigmentation. Maintaining and boosting healthy levels of Vitamin D is as easy as spending between five minutes and half an hour in the afternoon sun just a couple of days per week. Sunscreen with SPF 15 will reduce Vitamin D3 by 99% so it is important to not apply sunscreen during the five to thirty minute sessions in the sun.

Of course the sun is not the only source of Vitamin D. A variety of foods provide Vitamin D some of which are salmon, milk, breakfast cereals, eggs and portobello mushrooms. Supplements can also be used to boost Vitamin D levels and are effective.

lroot on August 14th, 2018

air pollution

A study conducted by a team of public health researchers and leading environmental engineers have determined that air pollution shortens the lives of humans by more than a year. This is the first study that looked at data from air pollution and lifespan in order to examine global variations on how they might affect overall life expectancy.

Outdoor air pollution was looked at from particulate matter (PM) smaller than 2.5 microns. Particles this fine can enter deep into the lungs and breathing these particles is associated with an increase risk of a variety of serious diseases and conditions. 2.5 microns is pollution that comes from car, trucks, fires, wind storms, power plants and industrial and agriculture emissions.

Led by researchers at the Cockrell School of Engineering at The University of Texas at Austin, data from the Global Burden of Disease Study was used to measure PM2.5 air pollution exposure and its affects in 185 countries. The team then quantified the national impact on lifespan for each individual country as well on a global scale. Their findings were published in the August 22nd issue of Environmental Science & Technology Letters.

Globally, outdoor air pollution reduces average life expectancy at birth by one year. The effect is more pronounced in some countries such as Egypt were life span is reduced by 1.9 years, in India by 1.5 years and in Russia it is about nine months. In heavily populated areas of Asia and Africa it is much worse with life expectancy between one year and two months to one year and eleven months. In the United States it is less, currently reducing average life expectancy of an American born today by just over four months.

The study took into account measurements of ambient or outdoor air pollution. Data was gathered from previous studies using ground based pollution meters and satellites to calculate levels of ambient particular matter (PM2.5). The lead researcher, Dr. Joshua Apte, called this kind of particular matter “the single more important environmental pollutant for ill health and death.” Right now 95% of the world’s population are exposed to levels of PM2.5 which exceed the World Health Organization’s recommended level.

From previous studies, data indicated that PM2.5 was the fifth highest mortality risk factor in 2015. Exposure to PM2.5 levels caused 4.2 millions deaths that year and 103.1 million life years lost after adjusting for disabilities. This is the equaivalent of 7.6% of all deaths world wide in 2015. The World Health Organization estimates that one in nine deaths are related to indoor and outdoor air pollution.

The study also discovered that death rates from air pollution had increase calculating 3.5 million people died worldwide from breathing PM2.5 in 1990 which is 700,000 fewer deaths compared to those killed in 2015. The researchers noted that the increase was most likely due to aging populations, changes in non communicable disease rates and the increase of air pollution in middle and low income countries.

It is well known that fine particle air pollution is a major worldwide killer. The study was able to systematically identify how air pollution substantially shortens lifespans throughout the world. Compared to other significant phenomena which affect human survival rates, Dr. Apte points out this is a significant large number even noting that it is considerably larger than the survival benefits that might be realized with cures found for both breast and lung cancer combined. In India and China the improvement of air quality would be especially large for the elderly. For a good portion of Asia reduced air pollution would affect 60 year old people by a 15 to 20 percent higher chance of living to 85 or older.

Dr. Apte reports that sources of PM2.5 pollution and greenhouse gas emissions are very often tightly linked. This means that moving to cleaner energy sources can deliver quick dividends for the health of the public. More efficient car and cleaner electricity directly affect both climate and health. He believes cleaner and more efficient energy use is one of the best added benefits of tackling climate change which will lead to healthier and longer lives.

To view the original scientific study click here: Ambient PM2.5 Reduces Global and Regional Life Expectancy.

stem cells 4

Research by the National University of Singapore and the FIRC Institute of Molecular Oncology in Italy has revealed that mature cells can be reprogrammed into redeployable stem cells without genetic engineering. This is important because there are significant health risks associated with treatment utilizing stem cells with added genes. Instead of direct genetic modification, they are instead confined to a defined geometric space for an extended period of time. The breakthrough findings will no doubt usher in a new generation of technologies for stem cell tissue engineering and regenerative medicine.

In earlier studies over a decade ago scientists showed that mature cells could be reprogrammed to become pluripotent stem cells which were capable of being developed into any cell type in the body. Scientists accomplished this by genetically modifying mature cells by introducing external factors that would reset genomic programs of the cells. This essentially turned back the clock returning them to an undifferentiated or unspecified state. These lab made cells which are known as induced pluripotent stem cells (iPSCs) could then be programmed into different types of cells for tissue repair, drug discovery and also to grow new organs for transplants. These cells did not need to be harvested from embryos.

Unfortunately a major problem is the tendency for any specialized cell that has been developed from iPSCs to form tumors after introduction into the body. The researchers turned their focus to understanding how stem cell growth and differentiation is regulated in the body and how cells naturally convert to another cell type or revert to an immature stem cell like state during tissue maintenance or during development.

The new research has shown that mature cells can be reprogrammed in vitro into pluripotent stem cells by confining the cells to a defined area for growth rather than generically modifying them.

When fibroblast cells which are a type of mature cell found in connective tissue such as ligaments and tendons were confined to rectangular areas, they very quickly assumed the shape of the the surface of the medium that they were attached to. This indicated the cells were responding and measuring to the physical properties of the environment then conveying this information to the nucleus where DNA genome programs and packaging would adapt accordingly.

The cells were grown over ten days until they formed spherical clusters of cells. The genetic analysis of the cells contained within these clusters revealed that specific characteristics of chromatin which is the condensed from of packaged DNA normally associated with mature fibroblasts were lost by the 6th day. At the 10th day the cells expressed genes which are normally associated with embryonic stem cells and iPSCs. They team learned that by confining the mature cells for an extended period the mature fibroblasts could be turned into pluripotent stem cells. To confirm, the researchers directed their growth with high efficiency into two different specialized cell types and some cells were also directed back into fibroblasts.

The physical parameters used are reflective of the transient geometric constraints that cells can be exposed to in the body. During development the establishment of niches and geometric patterns are essential to the formation of functional organs and tissues. When tissue is damaged through disease or injury, cells will experience sudden alterations to their environment. In these cases, mature cells might revert back to a pluripotent stem cell like state prior to being redeployed as specialized cells for maintenance and repair of tissue. The study shows for the first time that mechanical cues can reset genomic programs of mature cells and then return them to a pluripotent state.

The researchers believe the use of geometric constraints to reprogram mature cells might better reflect processes that naturally occur within the body. And more importantly, the findings allow researchers to generate stem cells from mature cells with high efficiency and without genetically modifying them.

To view the original scientific study click here: Laterally confined growth of cells induces nuclear reprogramming in the absence of exogenous biochemical factors

lroot on July 27th, 2018


A new study conducted at McGill University shows us that the bacteria which live in our intestinal tract have an influence on how well we age. The study focused on the how the intestinal microbiota influence longevity and aging. Composition of the intestinal tract and its effects on health have been studied in the past, however just recently has aging been associated with changes in the microbiota.

Sometimes the intestines are referred to as the human’s second brain. There are over 200 million neurons which innervate it and combined with the microbiota which is the ecosystem of fungi, bacteria and microorganisms which are present in the gastrointestinal tract, they form an entity which influences our emotions, our moods and also intervene in the development of neurological diseases. The brain along with the nervous system of the intestines and the intestinal microbiota communicate bidirectionally through the gut brain axis. Different types of information are transmitted including immunological, metabolic, neruonal and endocrine all of which are derived from bacterial cells and their metabolites.

Microbiota composition varies with age and these alterations have been shown to be associated with aging and disease development. The microbiota are able to simultaneously modulate age related processes such as oxidative stress, metabolite regulation, energy homeostasis and inflammation through the gut brain axis. Microbiota therefore have been identified as a therapy against age related diseases.

The researchers in the recent study analyzed what impact three probiotics and a new prebiotic would have on the lifespan of male fruit flies. Fruit flies are about 70% similar to mammals in terms of their biochemical pathways. The intestinal microbiota varied with age which were similar to those observed in humans. The combination of probiotics and prebiotics increased the longevity of male fruit flies by 60% and using just a probiotic combination alone increased longevity by 55%.

Researchers noted that similar results were realized with similar experiments on mice and rat models. The different mixtures of probiotics had beneficial effects against memory loss, neurodegeneration, antioxidant defenses, immunity and inflammation and increased lifespan in the mice. In additional studies, probiotics were observed to increase the lifespan of C elegans (roundworms).

To maintain a healthy intestinal microbiota to help delay chronic diseases and extend lifespan, a diet rich in probiotics and prebiotics is highly recommended. Symbiotic formulations which mix probiotics and prebiotics have shown beneficial results against age related biological disorders and also for anti aging. It is hoped that in the future specific symbiotic formulas can be developed to help prevent chronic and neurodegenerative diseases.

To view the original scientific study click here: Longevity extension in Drosophila through gut-brain communication

white blood cell

A research team at University of California San Francisco, has discovered how to genetically reprogram human cells without the use of viruses to insert DNA. The breakthrough technique has far reaching significance in medicine, research and industry. Using CRISPR gene editing technology in a versatile, rapid and economical approach, the team believes the technique will be adopted in the field of cell therapy which could accelerate the development of new and safer treatments for a variety of diseases.

The new method is a robust molecular “cut and paste” technique which was used to rewrite genome sequences in T cells. The technique relies on electroporation which is a process where an electrical field is applied to cells which makes their membranes temporarily more permeable. The UCSF team discovered that when certain quantities of T cells, DNA and CRISPR scissors were combined and then exposed to an appropriate electrical field, the T cells will absorb these elements and then integrate specific genetic sequences very precisely at the site of a CRISPR programmed cut in the genome.

The method is a rapid and flexible technique that can be used to enhance, reprogram and alter T cells which can be given specificity to a variety of diseases to tamp down excessive immune response. Just as important as the new technique’s ease of use and speed, the approach has made it possible to insert substantial stretches of DNA into T cells which will endow the cells with powerful new properties. Previously, some success had been achieved using electroporation and CRISPR to insert bits of genetic material into T cells, however not until the new research were they able to place long sequences of DNA into T cells without causing the cells to die leading them to believe DNA sequences were excessively toxic to T cells.

Through trial and error, the researchers determined the ratios of DNA quantity, T cell population and CRISPR abundance that when combined with an electrical field and delivered with proper parameters, the result was an accurate and efficient editing of the T cells genomes. To validate their findings, they directed CRISPR to label a variety of different T cell proteins with GFP (green fluorescent protein) and the outcome was very specific with very low levels of off target effects. T cells for this experiment were from three siblings with a rare and severe autoimmune disease. These children carry mutations in a gene called IL2RA.

To further serve as proof of principle of the new technique’s therapeutic promise, the team showed how it could possibly be used to marshall T cells against disease. Using a non viral CRISPR technique, the UCSF team were able to quickly repair the IL2RA defect in the children’s T cells and restore cellular signals that had been impaired by the mutations. Referred to as CAR-T therapy, T cells that have been removed from the body are engineered to improve their disease fighting abilities and then returned to the body.

In another set of experiments, the scientists were able to completely replace native T cell receptors in a population of normal human T cells with new receptors that had been engineered to find diseased cells. T cell receptors are cell sensors that detect disease or infection. In lab dishes the engineered cells were able to efficiently hone in on targeted disease cells while ignoring other cells which shows the sort of specificity that is a major goal in precision disease medicine. With the new technique, they are able to cut and paste into a specified place rewriting a specific page in the genome sequence.

The new technique has made is possible to create viable custom T cell lines in just over a week. Ideas for earlier experiments were deemed too expensive or difficult due to obstacles presented by viral vectors. Because they can create CRISPR templates very quickly, as soon as a template is created they can get it into T cells and grow them very rapidly which makes a variety of experiments now ripe for investigation.

To view the original scientific study click here: Reprogramming human T cell function and specificity with non-viral genome targeting

lroot on July 14th, 2018

coffee (2)

A new study conducted by a research team in Germany has found that four cups of coffee a day sets off a cellular chain of events that will protect the cells of our heart. By promoting the movement of a regulatory protein in mitochondria, function is enhanced and cardiovascular cells are protected from damage. Regulatory proteins bind to specific parts of DNA and play a role in how genes are expressed.

Mitochondria are referred to as the powerhouses of the cells and the benefits of caffeine seem to involve mitochondria. The researchers discovered a new player within mitochondria which is what appears to be relevant to caffeine’s protective effect: p27. P27 was first identified as an inhibitor of the cell cycle and is an enzyme that normally slows the division of cells. The team found that caffeine caused p27 to move into mitochondria. Once there, it triggered tasks vital for heart muscle repair after a heart attack. The team discovered that the equivalent of four or more espresso shots was sufficient to help protect from cell death, boosting processes to help the heart recover.

Previous studies have shown that caffeine consumption has been associated with lower risks for a variety of diseases, but the mechanism underlying these protective effects has not been clear. In the recent study, the team studied old, prediabetic, obese mice. The findings revealed that caffeine protected against heart damage in these mice. P27 promoted migration of endothelial cells, protected heart muscles from cell death and triggered conversion of fibroblasts into cells which contain contractile fibers which are all crucial for heart muscle repair after myocardial infraction.

The findings of the study should lead to better strategies for protecting the heart muscle from damage especially in the older populations. A new mode of action for caffeine could be one that promotes protection and repair of heart muscle through the action of p27. Enhancing mitochondrial p27 could also serve as a therapeutic strategy not only in cardiovascular disease but also in improving healthspan. The findings indicate that coffee can be part of a healthful diet.

To view the original scientific study click here: CDKN1B/p27 is localized in mitochondria and improves respiration-dependent processes in the cardiovascular system—New mode of action for caffeine

lroot on July 11th, 2018

girl walking fast

Exercise is an important part of staying healthy and maintaining a high quality of life. Now a new study shows that picking up the pace by walking faster can add years to a person’s life! The article published in the British Journal of Sports Medicine found that a fast or average speed of 3 to 4.5 mph cut the death risk by more than 20% over a 15 year period. The study conducted by the University of Sydney found that walkers who walked at a fast pace showed a decreased risk of cardiovascular disease and all cause mortality.

More than 50,000 walkers were included in the analysis. A fast walking pace may just be an easy, straightforward way to improve the health of the heart and reduce the risk of premature mortality. Data showed that brisk or walking at a fast pace reduced all cause mortality by 24%. Similar results were reported for decrease in cardiovascular disease. And the older a person is the more profound the effects can be. The study showed that those aged 60 or older who walked at a steady pace reduced their risk of heart disease by 46%. However those who walked at a fast pace reduced their risk by 53%.

Interestingly, the top five habits shown to increase an individuals lifespan by more than a decade are:

*Exercising an average of 30 minutes per day
*Abstaining from smoking
*Maintaining a BMI between 18.5 and 24.9
*Limiting alcohol consumption to no more than 15 grams per day for women and 30 grams per day for men
*Eating a diet low in red meat, sugars, saturated fats and high in vegetables, fruits & whole foods.

Walking at 3 to 4.5 mph is suggested. Another indicator that the speed is good is walking at a pace that makes you slightly out of breath and sweaty when sustained. Here are other tips for walking faster:

Use good posture by walking tall and looking forward. Chin should be level and your head up!

Keep your chest raised and shoulders down, back & relaxed

Bend your arms at a slightly less than 90 degree angle. Cup your hands and swing arms front to back – do not swing them side to side. Swinging your arms faster will get your feet to follow!

Tighten your abs and buttocks by flattening your back and tilting your pelvis slightly forward

Pretend you are walking a straight line instead of elongating your steps work at taking smaller, faster steps

Push off with your toes and concentrate on landing on your heel. Use the natural spring of your calf muscles to propel you forward

Breath naturally by taking deep rhythmic breaths to get the maximum amount of oxygen through your system. Walk fast enough that your breathing is faster than normal but not such that you are completely out of breath.

And some DON’T’S for walking healthy:
Do not over stride
Do not use too vigorous arm movements
Do not look at the ground
Do not hunch your shoulders
Do not carry hand weights on wear ankle weights

To view the original scientific study click here: Self-rated walking pace and all-cause, cardiovascular disease and cancer mortality: individual participant pooled analysis of 50 225 walkers from 11 population British cohorts


Researchers at the Stowers Institute for Medical Research have discovered the one cell that has the capability of regenerating an entire organism. Until recently scientists lacked the tools that could target and track this cell which enables a variety of creatures such as the planarian flatworm to perform amazing feats such as regrowing a severed head.

By pioneering a new technique that combines single cell analysis, flow cytometry, imaging and genomics, the researchers have isolated this regenerative cell which is a subtype of the earlier studied adult pluripotent stem cell before it performed this remarkable act. Now that this stem cell has been isolated prospectively the findings prove that this is no longer an abstraction. There really is a cellular entity that can restore to animals and humans the ability to regenerate any part of the body.

All multicellular organisms are built from a single cell which divides multiple times. Each of the cells has the exact same twisted strands of DNA and is considered pluripotent which means it can give rise to all cell type possibilities in the body. However somewhere along the way the starter cells which are known as embryonic stem cells find a different fate and become heart cells, muscle cells, skin cells and other types of cells. In humans no known pluripotent stem cells will remain after birth, however in planarians they remain into adulthood. Here they become known as adult pluripotent stem cells or neoblasts. It is believed these neoblasts contain the secret to regeneration.

It is only in the last 20 years that scientists have been able to characterize this powerful cell population using molecular techniques and functional assays. The work showed that this seemingly homogenous cell population was a conglomeration of different subtypes all with different patterns and properties of gene expression. Previous to the current study, scientists would have to transplant over a hundred single cells into the same amount of worms to find the one that is truly pluripotent and has the ability to regenerate the organism. Not only would that be a lot of work, but to define it molecularly by identifying the genes that cell is expressing they would have to destroy the cell for processing which meant not being able to keep the cell alive to track its regeneration.

The team began searching for a distinguishing characteristic that would identify this elusive cell ahead of time. A stem cell marker known as piwi 1 is able to distinguish neoblasts so the team decided to begin there. They first separated the cells that expressed this marker from the ones that did not. They then noticed the cells could be separated into two groups…one that expressed lower levels of piwi 1 and ones that expressed high levels of piwi 1. They found that the ones that were piwi 1 high were the ones that fit the molecular definition of neoblasts and so the other ones were discarded.

This type of gene expression and protein levels had never been conducted in planarians. Previously researchers believed all cells which expressed the piwi 1 were true neoblasts and it wasn’t relevant how much of the marker they expressed. The team showed it did make a difference.

The researchers selected 8,000+ of the high piwi 1 cells and proceeded to analyze their gene expression patterns. To their surprise, the cells fell into 12 different subgroups. Through elimination they excluded any subgroups that had genetic signatures indicating they were cells destined for a particular fate such as skin or muscle cells. That left them with two subgroups that could still be pluripotent. These two groups were called Nb1 and Nb2.

The cells in NB2 group expressed a gene coding for a member of the tetraspanin protein family which is a group of evolutionary ancient and also very poorly understood proteins that sit on the cell surface. They made an antibody that could latch onto this protein and pull the cells that carried it out of a mixture of other neoblasts. They then transplanted the single purified cell into a planarian which had been subjected to lethal levels of radiation. The cells not only repopulated and rescued the planarian, but they did so 14 times more consistently than cells which had been purified by older methods.

The fact that the marker the team discovered is expressed not only in planarians but also in humans, opens the door to new experiments never thought possible. It would make sense that these principles could be broadly applicable to any organism that has ever relied on stems cells to become what they are today. That is everybody!

To view the original scientific study click here: Prospectively Isolated Tetraspanin Neoblasts Are Adult Pluripotent Stem Cells Underlying Planaria Regeneration

lroot on July 1st, 2018


Researchers at the Perelman School of Medicine at the University of Pennsylvania along with the Plikus Laboratory for Development and Regenerative Biology at the University of California, Irvine, have discovered a way to heal wounds without scars by manipulating woulds to heal as regenerated skin. Previously thought to be impossible, the researchers have found a way to transform cells found in wounds into fat cells.

Adipocytes which are fat cells are typically found in the skin but they become lost when wounds heal as scars. Myofibroblasts are the most common cells found in wound healing which were thought to only form a scar. Scar tissue will not have hair follicles or fat cells which is what gives them their abnormal appearance. Using these characteristics, the researchers had the basis for their work which was comprised of changing the present myofibroblasts into fat cells which do not cause the typical scarring as the result of wound healing. The method was to regenerate hair follicles first then the fat would regenerate in response to those signals.

The study showed that fat and hair develop separately but not independently. Hair follicles will form first and the study discovered factors that were necessary for their formation. These additional factors were actually produced by the regenerating hair follicle converting surrounding myofibroblasts to regenerate as fat in place of a scar. This fat will not regenerate without the new hairs and once it does the new cells are indistinguishable from the existing fat cells giving the wound a more natural appearance.

The researchers identified a factor called Bone Morphogenetic Protein that sends the signal from the hair to the fat cells, instructing the myofibroblasts to turn into fat. This discovery alone was groundbreaking as it changed what was previously known about myofibroblasts. They were thought to be incapable of turning into a different type of cell. The study showed that they have the ability to influence cells and can be efficiently and stably converted into adipocytes. This transformation was shown in both mouse and human keloid cells which were grown in culture.

The discoveries show a great opportunity for wound healing to regenerate tissue rather than scarring. From a clinical standpoint the results are highly desirable and have the potential to revolutionize dermatology. Right now it is an unmet need.

The study also showed that the increase of fat cells in tissue might also be helpful for more than wound healing. Adipocyte loss is a fairly common complication of other conditions such as treatments for HIV and for the aging process when cells are lost naturally which leads to permanent deep wrinkles and discolouration.

To view the original scientific study click here: Regeneration of fat cells from myofibroblasts during wound healing