ArticleMediators of inflammation2018
Inhibition of the mTOR Pathway Exerts Cardioprotective Effects Partly through Autophagy in CLP Rats.
Article in Mediators of inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Hypoxia-Inducible Factor-1alpha/BNIP3-Mediated Mitochondrial Autophagy in Septic Cardiomyopathy: Protective Mechanism for Cardiac Function.Physiological research · 2026Article
- Review
- Roles of autophagy in sepsis-induced myocardial dysfunction: a comprehensive review.American journal of translational research · 2026Review
- mTOR/HIF-1α-associated scleral metabolic reprogramming by Mingshi formula in form-deprivation myopia.Scientific reports · 2025Article
- The endoplasmic reticulum stress status of CD4+ T lymphocytes and its association with mTOR-mediated autophagic-lysosomal disorder in elderly sepsis patients.Frontiers in immunology · 2025Observational
- Decoding Sepsis: Unraveling Key Signaling Pathways for Targeted Therapies.Research (Washington, D.C.) · 2025Review
- Rapamycin mitigates organ damage by autophagy-mediated NLRP3 inflammasome inactivation in sepsis.Histology and histopathology · 2024Article
- miR-29b-1-5p exacerbates myocardial injury induced by sepsis in a mouse model by targeting TERF2.Acta biochimica et biophysica Sinica · 2024Article
- mTOR signaling pathway regulation HIF-1 α effects on LPS induced intestinal mucosal epithelial model damage.BMC molecular and cell biology · 2024Article
- [HTD4010 attenuates myocardial injury in mice with septic cardiomyopathy by promoting autophagyNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Molecular hydrogen attenuates sepsis-induced cardiomyopathy in mice by promoting autophagy.BMC anesthesiology · 2024Article
- Regulated cell death pathways in cardiomyopathy.Acta pharmacologica Sinica · 2023Review
- Emerging roles of microRNAs in septic cardiomyopathy.Frontiers in pharmacology · 2023Review
- Modulation of the mTOR Pathway by Curcumin in the Heart of Septic Mice.Pharmaceutics · 2022Article
- mTOR pathway mediates endoplasmic reticulum stress-induced CD4Apoptosis : an international journal on programmed cell death · 2022Article
- Cardiomyocyte death in sepsis: Mechanisms and regulation (Review).Molecular medicine reports · 2022Review
- Canagliflozin attenuates lipotoxicity in cardiomyocytes and protects diabetic mouse hearts by inhibiting the mTOR/HIF-1α pathway.iScience · 2021Article
- UropathogenicFrontiers in immunology · 2021Article
- Inhibiting miR-22 Alleviates Cardiac Dysfunction by Regulating Sirt1 in Septic Cardiomyopathy.Frontiers in cell and developmental biology · 2021Article
- The Role of Autophagy in Sepsis: Protection and Injury to Organs.Frontiers in physiology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSepsis-induced myocardial dysfunction is a severe clinical problem. Recent studies have indicated that autophagy and myocardial energy depletion play a major role in myocardial dysfunction during sepsis, a mechanistic target of rapamycin (mTOR) as a master sensor of energy status and autophagy mediator; however, there are little data describing its role during sepsis in the heart.
methodsCecal ligation and puncture (CLP) or sham operation (SHAM) was performed in rats. After treatment, pathological changes were determined by H&E staining, cardiac functions by echocardiography, the distribution of microtubule-associated protein light chain 3 (LC-3) type II and hypoxia-inducible factor 1
resultsRapamycin alleviated the pathological damage of myocardial tissue, attenuated cardiac dysfunction (left ventricular ejection fraction (LVEF),
conclusionInhibition of the mTOR pathway has cardioprotective effects on myocardial dysfunction during sepsis induced by CLP, which is partly mediated through autophagy.
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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 OpenQuestion graph.