ArticleCell death & disease2018
Succinate induces aberrant mitochondrial fission in cardiomyocytes through GPR91 signaling.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 66 citations in OpenAlex.
- Mitochondrial Fusion and Fission in Age-Related Cardio-Cerebral Diseases: Mechanisms and Interventions.Aging cell · 2026Review
- Rebalancing mitochondrial dynamics restores succinate dehydrogenase activity and reduces succinate release in hepatocellular carcinoma.Journal of biomedical science · 2026Article
- Mechanisms Involved in Pathological Succinate-Mediated Signaling.International journal of molecular sciences · 2026Review
- Metabolic rewiring through succinate-GPR91 signaling: a fresh perspective on HFpEF energetics.Cardiovascular diabetology · 2026Article
- The role and therapeutic potential of succinate and succinylation in cardiovascular diseases.Clinical epigenetics · 2026Review
- Sensing succinate: SUCNR1 as a context-dependent metabolic and cellular signal integrator.Frontiers in molecular biosciences · 2026Review
- Succinate-GPR91 signaling promotes cardiomyocyte metabolic reprogramming and NADCardiovascular diabetology · 2025Article
- From Mechanisms to Diseases: The Succinate-GPR91 Axis in Cardiometabolic Diseases.Journal of cardiovascular translational research · 2025Review
- Succinate-GPR91 signaling promotes cardiomyocyte metabolic reprogramming and NADResearch square · 2025Article
- The role of redox signaling in mitochondria and endoplasmic reticulum regulation in kidney diseases.Archives of toxicology · 2025Review
- SDH defective cancers: molecular mechanisms and treatment strategies.Cell biology and toxicology · 2025Review
- DRP1, fission and apoptosis.Cell death discovery · 2025Review
- Increase in plasma succinate is associated with aerobic lactate production in a model of endotoxic shock.Experimental physiology · 2025Article
- Succinate in innate immunity: linking metabolic reprogramming to immune modulation.Frontiers in immunology · 2025Review
- Succinate Regulates Endothelial Mitochondrial Function and Barrier Integrity.Antioxidants (Basel, Switzerland) · 2024Article
- miR-369-3p ameliorates diabetes-associated atherosclerosis by regulating macrophage succinate-GPR91 signalling.Cardiovascular research · 2024Article
- The polyunsaturated fatty acid docosahexaenoic affects mitochondrial function in prostate cancer cells.Cancer & metabolism · 2024Article
- Early-life exercise induces immunometabolic epigenetic modification enhancing anti-inflammatory immunity in middle-aged male mice.Nature communications · 2024Article
- Impairment of substrate-mediated mitochondrial respiration in cardiac cells by chloroquine.Molecular and cellular biochemistry · 2024Article
- Mitochondrial damage and impaired mitophagy contribute to disease progression in SCA6.Acta neuropathologica · 2024Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Altered mitochondrial metabolism acts as an initial cause for cardiovascular diseases and metabolic intermediate succinate emerges as a mediator of mitochondrial dysfunction. This work aims to investigate whether or not extracellular succinate accumulation and its targeted G protein-coupled receptor-91 (GPR91) activation induce cardiac injury through mitochondrial impairment. The results showed that extracellular succinate promoted the translocation of dynamin-related protein 1 (Drp1) to mitochondria via protein kinase Cδ (PKCδ) activation, and induced mitochondrial fission factor (MFF) phosphorylation via extracellular signal-regulated kinases-1/2 (ERK1/2) activation in a GPR91-dependent manner. As a result, enhanced localization of MFF and Drp1 in mitochondria promoted mitochondrial fission, leading to mitochondrial dysfunction and cardiomyocyte apoptosis. We further showed that inhibition of succinate release and GPR91 signaling ameliorated oxygen-glucose deprivation-induced injury in cardiomyocytes and isoproterenol-induced myocardial ischemia injury in mice. Taken together, these results showed that in response to cardiac ischemia, succinate release activated GPR91 and induced mitochondrial fission via regulation of PKCδ and ERK1/2 signaling branches. These findings suggest that inhibition of extracellular succinate-mediated GPR91 activation might be a potential therapeutic strategy for protecting cardiomyocytes from ischemic injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.