Glycolytic Pathways Drive Systemic Inflammation in Dermatomyositis

METABOLIC reprogramming in the skin may fuel systemic inflammation in patients with dermatomyositis (DM), according to a new study, opening potential paths to novel therapies. Researchers used single-cell RNA sequencing and proteomic analysis to dissect the cellular landscape of DM skin lesions and link it to broader systemic immune activation.

Systemic Inflammation Rooted in Skin Fibroblasts

By mapping skin samples from adults with DM at single-cell resolution, the team uncovered that fibroblasts, not immune cells, emerge as the main signalling hub within inflamed skin. These so-called “inflammatory fibroblasts” showed strong activation of the type I interferon (IFN-I) pathway, a hallmark of immune dysregulation, and were linked to elevated expression of the chemokine CXCL10.

Importantly, the study identified a novel “CXCL10–glycolysis axis” as a core mechanism driving inflammation. Proteomic and transcriptomic data from both skin and blood suggested that increased glycolytic activity in inflammatory fibroblasts correlates with systemic inflammatory signals. This metabolic shift appears to amplify immune activation beyond the skin, linking local pathology to systemic disease burden.

In a preclinical model of autoimmune myositis, inhibiting glycolysis using 2‑deoxy‑D‑glucose (2DG) significantly reduced inflammation, supporting the idea that metabolic reprogramming is not just a bystander but a driver of disease. These findings suggest that targeting cellular metabolism, particularly glycolysis, might offer a promising new therapeutic avenue for DM.

Implications for Clinical Care and Future Research

The study challenges the traditional view that immune cells are the main culprits in DM skin inflammation, highlighting instead a central role for fibroblasts and metabolic dysfunction. The link between skin-level changes and systemic inflammation underscores the importance of holistic disease management. The authors call for further research into metabolism-targeted treatments and suggest integrating metabolomic and proteomic profiling into routine care to better stratify patients and personalise therapy.

 

 

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Sweet Tooth Gene Tied to Less Body Fat

A variant in the gene for a certain hormone is tied to people eating more carbs. Yet a new study of 451,000 people finds that the allele doesn’t universally mean poorer health. Researchers reported yesterday that those with the sweet-tooth variant actually have lower body fat than others, and no higher risk for type 2 diabetes. They did, however, find a link between the allele and high blood pressure and a thicker waistline.

“This goes against the current perception that eating sugar is bad for health. It may reduce body fat because the same allele also results in a lower consumption of protein and fat in the diet,” study coauthor, a molecular geneticist , says in a press release. “But whilst this version of the gene lowers body fat, it also redistributes fat to the upper body, where it’s more likely to cause harm, including higher blood pressure.”

The gene of interest here is FGF21, which encodes fibroblast growth factor 21, a hormone involved in alcohol and sugar consumption and insulin sensitization. The authors note that it’s a target of weight loss interventions.

People with a particular allele of FGF21—20 % of Europeans are homozygous for the variant—tend to consume relatively more sugar and alcohol than those without the allele. To see what consequences this might have on people’s health,the team  collected data on 451,000 people whose genetic and health information is part of the UK Biobank.

Although those with the sweet-tooth allele had less body fat than others, they had a higher waist-to-hip ratio. They also had higher blood pressure, but no greater risk for heart disease or type 2 diabetes. “These results suggest that FGF21 has pleiotropic effects, with separate effects on macronutrient intake to those on body shape and blood pressure,” the authors write in their report.

A nutrition scientist tells that the results may warrant a rethink of the idea that “no matter what, sugar consumption is bad. This villainisation needs proper exploration.”

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Scientists turn skin cells into stem cells that kill brain cancer

For the first time, scientists have turned skin cells into cancer-hunting stem cells that destroy brain tumors known as glioblastoma. The discovery could offer, for the first time in more than 30 years, a new and more effective treatment for the deadly disease.

The survival rate beyond two years for a patient with a glioblastoma is 30 percent because it is so difficult to treat. Even if a surgeon removes most of the tumor, it's nearly impossible to get the invasive, cancerous tendrils that spread deeper into the brain and inevitably the remnants grow back.

 

 The technique builds upon the newest version of the Nobel Prize-winning technology from 2007, which allowed researchers to turn skin cells into embryonic-like stem cells. Researchers hailed the possibilities for use in regenerative medicine and drug screening. Now, researchers have found a new use: killing brain cancer.
“Patients desperately need a better standard of care,” says a researcher.

 
The survival rate beyond two years for a patient with a glioblastoma is 30 percent because it is so difficult to treat. Even if a surgeon removes most of the tumor, it’s nearly impossible to get the invasive, cancerous tendrils that spread deeper into the brain and inevitably the remnants grow back. Most patients die within a year and a half of their diagnosis.
Researchers believe that developing a new personalized treatment for glioblastoma that starts with a patient’s own skin cells could improve those statistics, with a goal of getting rid of the cancerous tendrils, effectively killing the glioblastoma.

 

 For the new study, published in a journal , researchers reprogrammed skin cells known as fibroblasts—which produce collagen and connective tissue—to become induced neural stem cells. Working with mice, the team showed that these neural stem cells have an innate ability to move throughout the brain and home in on and kill any remaining cancer cells. The team also showed that the stem cells could be engineered to produce a tumor-killing protein, adding another blow to the cancer.
Depending on the type of tumor, the researchers increased survival time of the mice by 160 to 220 percent. Next steps will focus on human stem cells and testing more effective anti-cancer drugs that can be loaded into the tumor-seeking neural stem cells.
“Our work represents the newest evolution of the stem-cell technology that won said a researcher. “We wanted to find out if these induced neural stem cells would home in on cancer cells and whether they could be used to deliver a therapeutic agent. This is the first time this direct reprogramming technology has been used to treat cancer.”
The researchers are also currently improving the staying power of stem cells within the surgical cavity. They discovered that the stem cells needed a physical matrix to support and organize them, so they will hang around long enough to seek out the cancerous tendrils.

 

“Without a structure like that, the stem cells wander off too quickly to do any good,” says the scientist, who reported these findings.

For that study, researchers added stem cells to an FDA-approved fibrin sealant commonly used as surgical glue. The physical matrix it creates tripled the retention of stem cells in the surgical cavity, providing further support for the applicability and strength of the technique.

 

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Natural Process for Scar-free Wound Healing Developed

Scars are often the unwanted and permanent result of wound healing, but University of California, Irvine and University of Pennsylvania researchers have discovered a natural regeneration process that stimulates scar-free skin repair.

Their study results, which appear in Science, point the way toward possible clinical treatments for scar-free wound healing, a highly desirable yet unmet need.

UCI’s Maksim Plikus, Penn’s George Cotsarelis and their colleagues identified in mouse studies never-before-seen cellular and molecular processes in which large wounds in adult mice regenerated nearly normal-looking skin, complete with new hair follicles and fat tissue. Ultimately, the center of the wound became nearly indistinguishable from normal, unwounded skin.

How did this occur?

“Typically, myofibroblasts, the primary cell type found in wounds, were thought to be incapable of becoming other cell types. However, our team found that wound myofibroblasts can efficiently and stably convert into new distinct cell types, specifically new adipocytes, which are the fat-laden cells necessary for healthy skin,” explained Christian F. Guerrero-Juarez, a graduate student in Plikus’ lab who worked closely on the project.

Guerrero-Juarez said their study established that wounds with hair follicles produce the instructive factors that can reprogram myofibroblasts into adipocytes. Critical for driving the rewiring of cells’ identity is bone morphogenic protein signaling. In skin wounds, hair follicles secrete large amounts of these BMP molecules. The fact that hair follicles act as the natural source of BMPs explains why hairless wounds cannot regenerate adipocytes.
“Essentially, we can manipulate wound healing so that it leads to skin regeneration rather than scarring,” said Cotsarelis, chair of dermatology and Milton Bixler Hartzell Professor of Dermatology at Penn and principal investigator on the project. “The secret is to regenerate hair follicles first. After that, the fat will regenerate in response to the signals from those follicles.”

“In culture conditions, exposure of human fibroblasts derived from keloids, a type of skin scar, to either pure BMP or to human hair follicles is sufficient to drive their reprogramming toward new adipocytes. This shows that our findings from mice are translatable to humans,” said Plikus, an assistant professor of developmental & cell biology at UCI.

He noted that regenerating fat cells in skin can be beneficial for conditions beyond scarring. The process could potentially become a new anti-aging treatment, as the formation of deep wrinkles is thought to result from permanent loss of skin fat. Without underlying fat, the skin’s surface shrinks and wrinkles like a deflating balloon. Another recent study in Science, to which Plikus’ lab contributed, showed that, beyond their cosmetic value, fat cells possess strong antimicrobial properties that help skin fend off infection.

The next step is to translate these basic research findings into clinical approaches for treating healing wounds and aging skin in patients, but Plikus said it would take more time.

“Theoretically, this can be achieved via injections of signaling molecules directly inside the scar, such as with a small insulin syringe (similar to how Botox injections are now done),” he said. “Also, small-molecule agonists and antagonists that modulate signaling pathways critical for fat cell formation can be potentially developed into cream formulations.”

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New method to kill brain cancer with skin cells

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 In a first, researchers have developed a method to turn skin cells into cancer-hunting stem cells that can destroy brain tumours known as glioblastoma.

The discovery can offer, for the first time in more than 30 years, a new and more effective treatment for the disease, the study said.

"Patients desperately need a better standard of care," said Shawn Hingtgen, assistant professor at the University of North Carolina at Chapel Hill in the US.

The survival rate beyond two years for a patient with glioblastoma is 30 percent because it is so difficult to treat.

Even if a surgeon removes most of the tumour, it is nearly impossible to get the invasive, cancerous tendrils that spread deeper into the brain and inevitably the remnants grow back.

The new technique, reported in the journal Nature Communications, builds upon the newest version of the Nobel Prize-winning technology from 2007, which allowed researchers to turn skin cells into embryonic-like stem cells. 

 In their work, the research team reprogrammed skin cells known as fibroblasts - which produce collagen and connective tissue -- to become induced neural stem cells.


Working with mice, Hingtgen's team showed that these neural stem cells have an innate ability to move throughout the brain and home in on and kill any remaining cancer cells.

The team also showed that these stem cells could be engineered to produce a tumour-killing protein, adding another blow to the cancer.

Depending on the type of tumour, Hingtgen's team increased survival time of the mice from 160 to 220 percent.

The next steps will focus on human stem cells and testing more effective anti-cancer drugs that can be loaded into the tumour-seeking neural stem cells.