Mitochondrial Dysfunction in Chronic Limb Ischemic Myopathy

Abstract

Critical limb ischemia (CLI), the most advanced clinical manifestation of peripheral arterial disease (PAD), is associated with cycles of ischemia and reperfusion (I/R) that are thought to compromise the bioenergetics of mitochondria. However, the specific biochemical mechanism through which the mitochondrial dysfunctions occur have not been fully characterized. In this experiment, the left femoral arteries of mice (n=3) were ligated and excised, and tibial anterior muscles were harvested on day 7 and 14. The sections were stained for hematoxylin and eosin (H&E), succinate dehydrogenase (SDH), and cytochrome C oxidase (COX). The results show significant increase in centralized nuclei in injured muscles compared to contralateral controls. SDH and COX data were inconclusive. Future studies are expected to continue identifying key mechanisms that link oxidative damage and mitochondrial dysfunction to develop targeted therapies that aim to improve the compromised bioenergetics of mitochondria, improving the prognosis of PAD and CLI patients.