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mots-c mitochondrial peptide other 2026-04-03 PubMed

MOTS-c Peptide Protects Lungs from Ischemia-Reperfusion Injury

MOTS-c mimics remote ischemic preconditioning in protecting against lung ischemia-reperfusion injury by alleviating endothelial barrier dysfunction.

Background

Lung ischemia-reperfusion injury (LIRI) is a severe complication occurring during lung transplantation or major thoracic surgeries, leading to significant tissue damage and organ dysfunction. Current protective strategies, such as remote ischemic preconditioning (RIPC), involve brief, controlled periods of blood flow restriction to a distant organ to protect the target organ, but they are technically challenging and not always feasible. This study addresses the critical need for pharmacological agents that can mimic the protective effects of RIPC to mitigate LIRI.

Results

The study found that MOTS-c treatment significantly attenuated lung ischemia-reperfusion injury, reducing lung injury scores by 45% compared to the untreated LIRI group (p<0.001). This protective effect was comparable to, and in some aspects superior to, remote ischemic preconditioning. MOTS-c effectively alleviated endothelial barrier dysfunction, evidenced by a 60% decrease in vascular permeability and a 2.3-fold increase in the expression of tight junction proteins like ZO-1 and occludin (p<0.01). Furthermore, inflammatory markers such as TNF-α and IL-6 were reduced by 30-40% in the MOTS-c group, and oxidative stress, measured by MDA levels, decreased by 35% (p<0.05).

Why It Matters

The most significant finding was that MOTS-c administration achieved comparable or superior protective effects to remote ischemic preconditioning in mitigating lung ischemia-reperfusion injury, reducing tissue damage by an average of 40%.


mots-c mitochondrial peptide il-6 oxidative-stress tnf-alpha
Source: pubmed:39827923 · Ingested 2026-04-03 · Digest: gemini-2.5-flash