Nikhil Prasad Fact checked by:Thailand Medical News Team Jan 22, 2026 1 hour, 53 minutes ago
Medical News: Researchers have identified a surprising biological signal that may help explain why some people with COVID-19 develop life-threatening illness while others recover more smoothly. A new study shows that hormones released by skeletal muscles strongly reflect inflammation levels, lung damage, and oxygen loss in hospitalized COVID-19 patients, offering a clearer picture of disease severity that goes beyond traditional risk factors.
Muscle-released hormones were found to mirror inflammation lung damage and oxygen loss in severe COVID-19 patients
Researchers And Institutions Involved
The study was conducted by scientists from the Department of Pulmonology and Lung Cancers and the Department of Histology and Cytophysiology at Wrocław Medical University in Wrocław, Poland. The research team analyzed clinical and laboratory data from 99 adult patients admitted with PCR-confirmed COVID-19.
Why Muscle Hormones Are Important
Skeletal muscles are increasingly recognized as endocrine organs that release chemical messengers known as myokines. Two such myokines, irisin and myostatin, help regulate inflammation, metabolism, and muscle function. Because COVID-19 is marked by widespread inflammation and oxygen deprivation, researchers suspected these muscle-derived substances might be linked to how severely the disease progresses.
Key Findings on Irisin Levels
The study found that patients who were more severely ill at hospital admission had significantly higher blood levels of irisin. Elevated irisin was closely associated with extensive lung involvement on chest imaging, lower blood oxygen levels, and stronger inflammatory responses. Higher irisin levels also correlated with increased markers such as C-reactive protein, ferritin, D-dimers, and abnormal white blood cell ratios. Patients with irisin levels above the median were more likely to progress to critical illness or die. Notably, irisin levels fell in over 90 percent of patients during hospitalization, paralleling clinical improvement and declining inflammation.
What Myostatin Revealed
Myostatin showed a different but equally meaningful pattern. Higher myostatin levels at admission were linked to severe inflammation and a higher likelihood of progressing to critical COVID-19. Patients with elevated myostatin also tended to have poorer oxygen levels by the time of discharge. Unlike irisin, myostatin concentrations generally remained stable throughout hospitalization, though patients with the highest inflammatory burden at the start often showed a decline over time.
Understanding The Bigger Picture
These findings suggest that muscle tissue actively participates in the body’s response to severe viral infection. Rather than being protective signals alone, elevated irisin and myostatin appear to act as indicators of intense physiological stress, systemic inflammation, and oxygen deprivation. This
Medical News report highlights how muscle-derived hormones may serve as valuable b
iomarkers that reflect disease severity more accurately than body weight or age alone.
Clinical And Research Implications
The results indicate that monitoring muscle hormones could help clinicians better identify patients at risk of deterioration and track recovery during hospitalization. They also point to skeletal muscle as a potential therapeutic target, where preserving muscle health and regulating myokine release might improve outcomes in severe infections.
Conclusions
This study underscores that skeletal muscles are not passive during COVID-19 but play an active hormonal role in shaping inflammation and oxygen balance. Elevated irisin and myostatin levels signal severe disease, extensive lung involvement, and higher risk of critical outcomes. Understanding this muscle-immune interaction may lead to improved risk assessment tools and novel treatment strategies aimed at reducing inflammation, preserving muscle function, and improving survival in future respiratory pandemics.
The study findings were published in the peer reviewed journal: Frontiers in Endocrinology.
https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2025.1668035/full
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