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Article Abstract
This study investigates the role of c-FLIP in sepsis-induced myocardial dysfunction (SIMD), focusing on cardiac microcirculation and mitochondrial autophagy. Using SIMD rat and LPS-induced cardiac microvascular endothelial cell injury models, we found that c-FLIP deficiency disrupts mitochondrial homeostasis, exacerbating microcirculatory damage. c-FLIP differentially regulates mitochondrial autophagy via FUNDC1. Overexpression of c-FLIP balances autophagy, protects mitochondria, reduces inflammation, and ameliorates SIMD, highlighting its potential as a therapeutic target.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12399170 | PMC |
| http://dx.doi.org/10.1016/j.jacbts.2025.02.016 | DOI Listing |
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