ArticleFrontiers in cardiovascular medicine2026
Mechanisms underlying the reversal of hypoxia-induced energy metabolic reprogramming in cardiomyocytes by Poria cocos triterpenoids: integrated regulation of mitochondrial dynamics and the autophagy-lysosomal pathway.
Article in Frontiers in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: To elucidate the mechanisms by which Poria cocos triterpenoids reverse hypoxia-induced energy metabolic reprogramming in cardiomyocytes through integrated regulation of mitochondrial dynamics and the autophagy-lysosomal pathway. Methods: A hypoxic injury model was established in H9c2 rat cardiomyoblasts. Cells were randomized into five groups: normal control, hypoxia model, and low-, medium-, and high-dose Poria cocos triterpenoid-treated groups. Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay. Western blotting quantified protein expression levels of mitochondrial fusion (Mfn1, Mfn2, OPA1) and fission (Drp1, Fis1) regulators; autophagy-lysosomal markers (LC3-II/I ratio, p62, PINK1, Parkin, LAMP1, ATG5); and key metabolic enzymes (CPT1, PFK-2). Mitochondrial respiratory control ratio (RCR) and ATP production rate were measured via high-resolution respirometry; extracellular acidification rate (ECAR), oxygen consumption rate (OCR), and fatty acid oxidation (FAO) efficiency were determined using Seahorse XF Analyzer. Intracellular lactate and pyruvate concentrations were quantified enzymatically. Functional validation employed siRNA-mediated knockdown of Drp1 or ATG5 to assess mechanistic dependency. Results: Compared with the normal control group, the hypoxia model group exhibited significantly reduced cell viability ( Conclusion: Poria cocos triterpenoids restore energy homeostasis in hypoxic cardiomyocytes by concurrently normalizing Drp1-mediated mitochondrial fission and ATG5-dependent autophagic clearance. This dual regulation rescues mitochondrial structural integrity, enhances oxidative phosphorylation, suppresses pathological glycolysis, and thereby reverses hypoxia-induced metabolic reprogramming-ultimately preserving cardiomyocyte viability.
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