ArticleActa biochimica et biophysica Sinica2025
Succinate accumulation induces pyroptosis and mitochondrial damage via the inhibition of ATP5F1D in HUVECs.
Article in Acta biochimica et biophysica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Shaping death: how the microbiome regulates tumour cell demise and therapy response.Cancer metastasis reviews · 2026Review
- Gut-heart axis at high altitude: a dynamic mediator from hypoxic dysbiosis to adaptive cardioprotection.Frontiers in microbiology · 2026Review
- Delving into pyroptosis in atherosclerosis: role, mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
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Authors and funding
10 authors.
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Abstract
Atherosclerosis, a chronic inflammatory disorder, is pathophysiologically linked to endothelial cell (EC) pyroptosis. This study aims to elucidate the mechanisms by which succinate exacerbates EC pyroptosis through mitochondrial damage. Serum samples are collected from patients with coronary heart disease (CHD) and healthy controls (HCs), and the levels of succinate, interleukin (IL)-6, and IL-18 are quantified. To establish a succinate accumulation model, human umbilical vein endothelial cells (HUVECs) are treated with diethyl butyl malonate (DEBM), followed by analysis of inflammatory cytokines. The expression of pyroptosis-related proteins is assessed via western blot analysis. Morphological changes in pyroptotic vesicles and membrane pores are examined by scanning electron microscopy (SEM) and transmission electron microscopy (TEM). The mitochondrial membrane potential and reactive oxygen species (ROS) levels are evaluated via a JC-1 kit and MitoSOX, respectively. RNA sequencing (RNA-seq) is performed to identify potential target genes and regulatory pathways. To investigate the functional role of ATP5F1D, small interfering RNAs (siRNAs) are used to knockdown
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