ArticleJournal of cellular and molecular medicine2021
CircTLK1 modulates sepsis-induced cardiomyocyte apoptosis via enhancing PARP1/HMGB1 axis-mediated mitochondrial DNA damage by sponging miR-17-5p.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- MicroRNAs as regulators of cardiac dysfunction in sepsis: pathogenesis and diagnostic potential.Frontiers in cardiovascular medicine · 2025Pooled it
- ROS-ATM-CBP axis-mediated PARP1 lactylation aggravates doxorubicin-induced cardiotoxicity.Clinical and translational medicine · 2026Article
- Epigenetic Mechanisms in Sepsis-Induced Cardiomyopathy: From Pathophysiology to Therapeutic Targets.International journal of molecular sciences · 2026Review
- Overexpression of Circular RNA circTTN Promotes Ferroptosis in Sepsis-Induced Cardiomyopathy.Journal of cellular and molecular medicine · 2026Article
- mRedox biology · 2026Review
- Therapeutic potential of ADAR1-regulated macrophage exosomes for improving myocardial damage in septic cardiomyopathy.Journal of nanobiotechnology · 2026Article
- Therapeutical progress in sepsis-induced cardiomyopathy.Frontiers in cardiovascular medicine · 2026Review
- HMGB1: a multifaceted mediator of cell death pathways in cardiovascular diseases.Apoptosis : an international journal on programmed cell death · 2025Review
- CAFs-derived Exosomal miR-889-3p Might Repress M1 Macrophage Polarization to Boost ESCC Development by Regulating STAT1.Cell biochemistry and biophysics · 2025Article
- Downregulation of circTLK1 improves the impairments in learning and memory induced by anesthetics via regulating miR-374b-5p expression and reducing neuroinflammation.Toxicology research · 2024Article
- Circular RNAs: a small piece in the heart failure puzzle.Functional & integrative genomics · 2024Review
- High expression circRALGPS2 in atretic follicle induces chicken granulosa cell apoptosis and autophagy via encoding a new protein.Journal of animal science and biotechnology · 2024Article
- Neutrophil extracellular traps mediate cardiomyocyte ferroptosis via the Hippo-Yap pathway to exacerbate doxorubicin-induced cardiotoxicity.Cellular and molecular life sciences : CMLS · 2024Article
- Revealing Landscape of Competing Endogenous RNA Networks in Sepsis-Induced Cardiovascular Diseases.Reviews in cardiovascular medicine · 2023Review
- CircRNAs regulate the crosstalk between inflammation and tumorigenesis: The bilateral association and molecular mechanisms.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Review
- PARP1 Activation Induces HMGB1 Secretion Promoting Intestinal Inflammation in Mice and Human Intestinal Organoids.International journal of molecular sciences · 2023Article
- Emerging roles of microRNAs in septic cardiomyopathy.Frontiers in pharmacology · 2023Review
- Serine/threonine kinase 3 promotes oxidative stress and mitochondrial damage in septic cardiomyopathy through inducing Kelch-like ECH-associated protein 1 phosphorylation and nuclear factor erythroid 2-related factor 2 degradation.International journal of biological sciences · 2023Article
- The role of E3 ubiquitin ligase WWP2 and the regulation of PARP1 by ubiquitinated degradation in acute lymphoblastic leukemia.Cell death discovery · 2022Article
- MiR-501-5p alleviates cardiac dysfunction in septic patients through targeting NR4A3 to prevent its binding with Bcl-2.Cell cycle (Georgetown, Tex.) · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionSeptic cardiomyopathy is a common complication of sepsis with high morbidity and mortality, but lacks specific therapy. This study aimed to reveal the role of circTLK1 and its potential mechanisms in septic cardiomyopathy. MATERIALS AND
methodsThe in vitro and in vivo models of septic cardiomyopathy were established. Cell viability and apoptosis were detected by CCK8, TUNEL and flow cytometry, respectively. LDH, CK, SOD, MDA, ATP, 8-OHdG, NAD+/NADH ratio, ROS level, mitochondrial membrane potential and cytochrome C distribution were evaluated using commercial kits. qRT-PCR and western blotting were performed to detect RNA and protein levels. Mitochondrial DNA (mtDNA) copy number and transcription were assessed by quantitative PCR. Dual-luciferase assay, RNA immunoprecipitation and co-immunoprecipitation were performed to verify the interaction between circTLK1/PARP1 and miR-17-5p.
resultsCircTLK1, PARP1 and HMGB1 were up-regulated in the in vitro and in vivo models of septic cardiomyopathy. CircTLK1 inhibition restrained LPS-induced up-regulation of PARP1 and HMGB1. Moreover, circTLK1 knockdown repressed sepsis-induced mtDNA oxidative damage, mitochondrial dysfunction and consequent cardiomyocyte apoptosis by inhibiting PARP1/HMGB1 axis in vitro and in vivo. In addition, circTLK1 enhanced PARP1 expression via sponging miR-17-5p. Inhibition of miR-17-5p abolished the protective effects of circTLK1 silencing on oxidative mtDNA damage and cardiomyocyte apoptosis.
conclusionCircTLK1 sponged miR-17-5p to aggravate mtDNA oxidative damage, mitochondrial dysfunction and cardiomyocyte apoptosis via activating PARP1/HMGB1 axis during sepsis, indicating that circTLK1 may be a putative therapeutic target for septic cardiomyopathy.
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Registered trials
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