What this means
This is a review of earlier work on a small protein made by mitochondria. It finds the idea plausible but not yet well tested in sepsis-related heart damage.
Plain-English summary written by an AI model from the abstract. The original is below.
- Who it was tested in
- A review of earlier studies; no new tests reported
- Kind of research
- A summary of earlier studies
The science
- Original title
- MOTS-c in sepsis-induced cardiomyopathy: Mechanisms and translational potential.
- Authors
- Zhao Z, Chen W, Zheng X et al.
- Journal
- European journal of pharmacology
- Published
- Aug 23, 2026
- Study type
- Review · in humans
- PMID
- 42633878 ↗
Abstract
Sepsis-induced cardiomyopathy (SICM) is a prevalent cardiac complication of sepsis that is characterized by inflammatory dysregulation, mitochondrial dysfunction, metabolic disturbance, and changes in the myocardial microenvironment. Mitochondrial open reading frame of the 12S rRNA type-c (MOTS-c) is a mitochondrial-derived microprotein with metabolic regulatory and stress-responsive properties. Existing studies have linked MOTS-c to AMP-activated protein kinase-related energy metabolism, antioxidant responses, inflammatory restraint, endothelial and microvascular protection, and mitochondrial quality control. These processes are relevant to SICM; however, there is limited direct SICM-specific evidence for MOTS-c, and several proposed mechanisms, such as stress-responsive nuclear signaling, have been established primarily in non-SICM settings. This review summarizes the biological characteristics and stress-responsive regulation of MOTS-c, evaluates its potential involvement in pathological processes related to SICM, and distinguishes direct SICM evidence from findings extrapolated from other cardiovascular, metabolic, and inflammatory disease models. We also discuss the exploratory value and current limitations of MOTS-c as a stress-related adjunctive biomarker and potential therapeutic candidate, with particular attention to biomarker specificity, post-treatment efficacy, target-cell mechanisms, and pharmacokinetic or biodistribution issues under septic conditions. Overall, MOTS-c represents a plausible but insufficiently validated molecule in SICM research, and its translational relevance will depend on disease-specific mechanistic and pharmacological validation.
Zhao Z, Chen W, Zheng X et al. MOTS-c in sepsis-induced cardiomyopathy: Mechanisms and translational potential. European journal of pharmacology. 2026. doi:10.1016/j.ejphar.2026.179261. PMID: 42633878. https://pubmed.ncbi.nlm.nih.gov/42633878/
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