Medical Bulletin 22/January/2026

Heart attacks occur when blood flow to the heart is blocked, causing large numbers of heart muscle cells to die. Traditionally, scientists believed these lost cells were replaced only by scar tissue, permanently weakening the heart’s ability to pump blood. While limited heart muscle regeneration had been observed in animals like mice, it had never been clearly demonstrated in humans—until now.

To uncover this phenomenon, the research team analyzed living heart tissue collected from patients undergoing bypass surgery at Royal Prince Alfred Hospital in Sydney. Using advanced cellular and molecular techniques, they examined these samples for signs of mitosis—the process by which cells divide to create new cells. The scientists found clear evidence that, alongside scar formation, new heart muscle cells were being produced in areas affected by a previous heart attack.

Robert Hume, the study’s first author, explained that these finding overturns long-held assumptions about heart damage being permanent. While the regenerated cells do not fully replace all lost tissue, their presence proves that the human heart retains some natural repair capacity.

The study’s senior author, Professor Sean Lal, emphasized that the real promise lies ahead. By understanding how and why these new cells form, scientists hope to develop treatments that can boost this natural process, encouraging the heart to regenerate more effectively after injury.

This discovery provides crucial groundwork for regenerative medicine, offering fresh hope that future therapies could help the heart heal itself—transforming how heart disease is treated in the years to come.

REFERENCE: Hume, Robert D. et al.; Human Hearts Intrinsically Increase Cardiomyocyte Mitosis After Myocardial Infarction; Circulation Research; doi: 10.1161/CIRCRESAHA.125.327486

Study Shows Aged Sperm RNA Alters Cellular Metabolism in Offspring

As more people choose to start families later in life, scientists are racing to understand how a father’s age might quietly shape the health of the next generation. A new study now suggests that the answer may lie not just in DNA, but in a lesser-known molecular messenger carried by sperm: RNA.

RNA plays a critical role in regulating how genes are switched on and off, especially during early development. In this study, published in The EMBO Journal, scientists used a newly developed sequencing technique called PANDORA-seq, designed to detect types of sperm RNA that standard methods often miss. This advanced approach allowed them to observe patterns that had remained invisible until now.

For years, research has shown that increasing paternal age is linked to higher risks in children, including obesity, metabolic disorders, and even stillbirth. Until now, most explanations focused on age-related damage to sperm DNA. But researchers at University of Utah Health have uncovered a new layer to this story, revealing that sperm RNA changes dramatically with age—and in surprisingly similar ways in both mice and humans.

When the team analyzed mouse sperm, they found a striking “aging cliff”—a rapid shift in RNA composition occurring at mid-life. Alongside this sudden transition, they identified what appears to be a molecular clock: as males age, certain sperm RNAs gradually become longer, while shorter RNA fragments decline. When researchers examined human sperm, they found the same progressive lengthening pattern, suggesting a conserved biological process across species.

This discovery was unexpected. While aging is known to fragment sperm DNA, the researchers found that specific RNAs actually grow longer over time. Importantly, these changes were most clearly seen in the sperm head—the part that enters the egg—highlighting their potential relevance for offspring development.

To explore possible consequences, the team introduced “old” sperm RNA into mouse embryonic stem cells. The cells showed altered gene activity linked to metabolism and neurodegeneration, offering a possible explanation for how paternal age might influence long-term health outcomes in children.

In the future, understanding and potentially targeting these RNA changes could lead to better diagnostics, improved fertility counseling, and healthier outcomes for families—no matter when parenthood begins.

REFERENCE: Shi, J., et al. (2026). Conserved shifts in sperm small non-coding RNA profiles during mouse and human aging. The EMBO Journal. DOI: 10.1038/s44318-025-00687-8. https://link.springer.com/article/10.1038/s44318-025-00687-8.

Diabetes Doubles Liver Damage Risk, Posing Major Public Health Crisis in India: Study

For millions of people, diabetes and fatty liver disease often exist quietly—causing little pain, few warning signs, and going undetected for years. But new research from India shows that when these two common conditions occur together, they can form a dangerous combination that sharply increases the risk of severe liver damage. The findings were published in the Journal of Clinical and Experimental Hepatology.

A large nationwide study conducted across 30 hospitals in India has found that people who have both diabetes and metabolic dysfunction–associated steatotic liver disease (MASLD), the new term for non-alcoholic fatty liver disease, face nearly double the risk of developing advanced liver scarring. This scarring, known as advanced fibrosis, can progress to cirrhosis, liver failure, or even liver cancer if left untreated.

MASLD and diabetes are both linked to problems in how the body handles sugar and fat. Each condition increases the likelihood of developing the other, but until now, scientists did not clearly understand how dangerous their coexistence could be. Given that fatty liver disease affects about one in three Indian adults and diabetes affects roughly one in ten, the combined risk represents a major public health concern.

To investigate this link, researchers from the Indian Consortium on MASLD followed thousands of patients across multiple cities for nearly five years. For this specific analysis, they closely examined 400 patients whose fatty liver disease had been confirmed through liver biopsy. Among them, 93 patients also had diabetes. The results were striking: 34 percent of patients with both conditions showed advanced fibrosis, compared to just 16.6 percent of those with MASLD alone—indicating a two-fold increase in risk.

According to lead investigator Dr. Ajay Duseja of PGIMER Chandigarh, not all fatty liver disease progresses in the same way. Some patients may remain stable for years. However, the presence of diabetes significantly accelerates liver damage and raises the chances of severe outcomes.

Supporting evidence from other Indian and international studies shows that patients with both diabetes and MASLD experience higher rates of liver complications, premature death, and reduced quality of life.

Early detection, good blood sugar control, and integrated treatment strategies could play a crucial role in preventing silent liver damage before it becomes life-threatening.

REFERENCE: Duseja, Ajay et al.; Indian National Association for Study of the Liver (INASL) Guidance Paper on Nomenclature, Diagnosis and Treatment of Nonalcoholic Fatty Liver Disease (NAFLD); Journal of Clinical and Experimental Hepatology, Volume 13, Issue 2, 273 – 302; DOI: 10.1016/j.jceh.2022.11.014