MOTS-c in sepsis-induced cardiomyopathy: Mechanisms and translational potential
This review concludes that MOTS-c is a plausible but insufficiently validated molecule for sepsis-induced cardiomyopathy; it may influence energy metabolism, inflammation, mitochondrial quality control, and endothelial protection, but direct SICM-specific evidence is limited. The paper maps proposed mechanisms and separates direct SICM findings from extrapolations based on other disease models.
Narrative review — Review.
Researchers studying MOTS-c will find a synthesis of its stress-responsive biology and a mapping onto SICM pathological processes, with explicit separation of direct SICM evidence from cross-disease extrapolation. The paper does not establish MOTS-c as an effective therapy or validated biomarker in SICM.
Key findings
MOTS-c is linked to AMPK-related energy metabolism, antioxidant responses, inflammatory restraint, endothelial and microvascular protection, and mitochondrial quality control.
Direct SICM-specific evidence for MOTS-c is limited, and several proposed mechanisms have been established primarily in non-SICM settings.
The review distinguishes direct SICM evidence from findings extrapolated from other cardiovascular, metabolic, and inflammatory disease models.
The authors identify biomarker specificity, post-treatment efficacy, target-cell mechanisms, and pharmacokinetic or biodistribution issues as unresolved for MOTS-c under septic conditions.
Limitations
Direct SICM-specific evidence for MOTS-c is limited.
Several proposed mechanisms were established primarily in non-SICM settings, so extrapolation to SICM is uncertain.
Biomarker specificity, post-treatment efficacy, target-cell mechanisms, and pharmacokinetic or biodistribution issues under septic conditions remain unresolved.
As a review, it provides no new experimental or clinical data.