ArticleAnnals of translational medicine2021
The effects of UCP2 on autophagy through the AMPK signaling pathway in septic cardiomyopathy and the underlying mechanism.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Exercise-Induced Exerkines Modulate Autophagy: Implications for Interorgan Crosstalk in the Hallmarks of Ageing.International journal of molecular sciences · 2026Review
- Erratum: The effects of UCP2 on autophagy through the AMPK signaling pathway in septic cardiomyopathy and the underlying mechanism.Annals of translational medicine · 2025Article
- Effects of simvastatin pretreatment on platelet activation and hypercoagulable state in septic mice.European journal of medical research · 2025Article
- FGF2 Attenuated Inflammation-Mediated Cardiac Damage: A Novel Mechanistic Insight into the AMPK-FUNDC1-Mitophagy.Research (Washington, D.C.) · 2025Article
- The Molecular Mechanisms of Imatinib Treatment on Acute Lung Injury in Septic Mice Through Proteomic Technology.Journal of immunology research · 2025Article
- Association of vascular netosis with COVID-19 severity in asymptomatic and symptomatic patients.iScience · 2024Article
- Article
- Sex-biased autophagy as a potential mechanism mediating sex differences in ischemic stroke outcome.Neural regeneration research · 2023Review
- Current insight on the mechanisms of programmed cell death in sepsis-induced myocardial dysfunction.Frontiers in cell and developmental biology · 2023Review
- Machine learning and bioinformatics to identify 8 autophagy-related biomarkers and construct gene regulatory networks in dilated cardiomyopathy.Scientific reports · 2022Article
- Metabolic reprogramming consequences of sepsis: adaptations and contradictions.Cellular and molecular life sciences : CMLS · 2022Review
- Research Progress on the Mechanism of Sepsis Induced Myocardial Injury.Journal of inflammation research · 2022Review
- Neuroplasticity to autophagy cross-talk in a therapeutic effect of physical exercises and irisin in ADHD.Frontiers in molecular neuroscience · 2022Review
- CAMKK2 regulates mitochondrial function by controlling succinate dehydrogenase expression, post-translational modification, megacomplex assembly, and activity in a cell-type-specific manner.Cell communication and signaling : CCS · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMitochondrial dysfunction plays an important role in the development of septic cardiomyopathy. This study aimed to reveal the protective role of uncoupling protein 2 (UCP2) in mitochondria through AMP-activated protein kinase (AMPK) on autophagy during septic cardiomyopathy.
methodsUCP2 knockout mice via a cecal ligation and puncture (CLP) model and the H9C2 cardiomyocyte cell line in response to lipopolysaccharide (LPS)
resultsCompared with the wild-type mice, the UCP2 knockout mice exhibited more severe cardiomyocyte injury after CLP, and the AMPK agonist AICAR protected against such injury. Consistent with this result, silencing UCP2 augmented the LPS-induced pathological damage and mitochondrial injury in the H9C2 cells, limited the upregulation of autophagy proteins and reduced AMPK phosphorylation. AICAR protected the cells from morphological changes and mitochondrial membrane potential loss and promoted autophagy. The silencing and overexpression of UCP2 led to correlated changes in the AMPK upstream kinases pLKB1 and CAMKK2.
conclusionsUCP2 exerts cardioprotective effects on mitochondrial dysfunction during sepsis via the action of AMPK on autophagy.
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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.