ArticleJournal of molecular and cellular cardiology2020
Defining decreased protein succinylation of failing human cardiac myofibrils in ischemic cardiomyopathy.
Article in Journal of molecular and cellular cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 51 citations in OpenAlex.
- G3BP1 Succinylation at K413 is Critical for Cardiac Function by Modulating PI3K-AKT-mTOR Signal Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cardiometabolic reprogramming in pulmonary arterial hypertension: Implications for right ventricular dysfunction and therapeutic strategies.Chinese herbal medicines · 2026Review
- The significance of the ketolytic gene OXCT1 in metabolism, intracellular signaling and disease development.Cellular and molecular life sciences : CMLS · 2026Review
- ATP5A1 succinylation as a key driver for the transition of myocardial ischemia to development of heart failure.Basic research in cardiology · 2026Article
- Beyond sarcomere genetics: proteomic insights into hypertrophic cardiomyopathy.Biophysical reviews · 2026Review
- Mechanisms Involved in Pathological Succinate-Mediated Signaling.International journal of molecular sciences · 2026Review
- Unveiling the importance of SIRT5 for cardiac health and disease in an era of increasing longevity.GeroScience · 2026Review
- Capturing Cardiomyocyte Cell-to-Cell Heterogeneity via Shotgun Single Cell Top-Down Proteomics.bioRxiv : the preprint server for biology · 2026Article
- The role and therapeutic potential of succinate and succinylation in cardiovascular diseases.Clinical epigenetics · 2026Review
- The function and mechanism of protein acylation in the regulation of viral infection.Virulence · 2025Review
- Post-translational acylation of proteins in cardiac hypertrophy.Nature reviews. Cardiology · 2025Review
- Global Proteoform Alterations Across Multiple Cellular Compartments Underlie Obstructive Hypertrophic Cardiomyopathy.Circulation. Heart failure · 2025Article
- Succinylation regulates boar sperm linear motility via reprogramming glucose metabolism.Communications biology · 2025Article
- Identification of GDP as a small inhibitory molecule in HepG2 cells by non‑targeted metabolomics analysis.Oncology letters · 2025Article
- Phosphorylation of CRYAB induces a condensatopathy to worsen post-myocardial infarction left ventricular remodeling.The Journal of clinical investigation · 2025Article
- Electro-acupuncture Suppresses Ferroptosis to Alleviate Cerebral Ischemia-Reperfusion Injury Through KAT3B-Mediated Succinylation of ACSL4.Applied biochemistry and biotechnology · 2025Article
- De-succinylation-induced accumulation of TRMT10C in the nucleus plays a detrimental role in coronary microembolization via its m1A modification function.International journal of biological sciences · 2025Article
- Quantifying Protein Acetylation in Diabetic Nephropathy from Formalin-Fixed Paraffin-Embedded Tissue.Proteomics. Clinical applications · 2024Article
- Sirtuin 5-Mediated Desuccinylation of ALDH2 Alleviates Mitochondrial Oxidative Stress Following Acetaminophen-Induced Acute Liver Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Succinylation modification: a potential therapeutic target in stroke.Neural regeneration research · 2024Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Succinylation is a post-translational modification of protein lysine residues with succinyl groups derived from succinyl CoA. Succinylation is considered a significant post-translational modification with the potential to impact protein function which is highly conserved across numerous species. The role of succinylation in the heart, especially in heart failure and myofibril mechanics, remains largely unexplored. Mechanical parameters were measured in myofibrils isolated from failing hearts of ischemic cardiomyopathy patients and non-failing donor controls. We employed mass spectrometry to quantify differential protein expression in myofibrils from failing ischemic cardiomyopathy hearts compared to non-failing hearts. In addition, we combined peptide enrichment by immunoprecipitation with liquid chromatography tandem mass spectrometry to quantitatively analyze succinylated lysine residues in these myofibrils. Several key parameters of sarcomeric mechanical interactions were altered in myofibrils isolated from failing ischemic cardiomyopathy hearts, including lower resting tension and a faster rate of activation. Of the 100 differentially expressed proteins, 46 showed increased expression in ischemic heart failure, while 54 demonstrated decreased expression in ischemic heart failure. Our quantitative succinylome analysis identified a total of 572 unique succinylated lysine sites located on 181 proteins, with 307 significantly changed succinylation events. We found that 297 succinyl-Lys demonstrated decreased succinylation on 104 proteins, while 10 residues demonstrated increased succinylation on 4 proteins. Investigating succinyl CoA generation, enzyme activity assays demonstrated that α-ketoglutarate dehydrogenase and succinate dehydrogenase activities were significantly decreased in ischemic heart failure. An activity assay for succinyl CoA synthetase demonstrated a significant increase in ischemic heart failure. Taken together, our findings support the hypothesis that succinyl CoA production is decreased and succinyl CoA turnover is increased in ischemic heart failure, potentially resulting in an overall decrease in the mitochondrial succinyl CoA pool, which may contribute to decreased myofibril protein succinylation in heart failure.
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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 Socratic graph.