ArticleOxidative medicine and cellular longevity2017
Brain-Derived Neurotrophic Factor Attenuates Septic Myocardial Dysfunction via eNOS/NO Pathway in Rats.
Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Impact of Chronic Mild Stress on Neurotrophic and Hypothalamic-Pituitary-Adrenal Factors in the Brain of Rats Submitted to Sepsis.Neurotoxicity research · 2026Article
- Natural products as multi‑target therapies for sepsis‑induced myocardial dysfunction (Review).International journal of molecular medicine · 2026Review
- BDNF-induced BDNF release: A virtuous loop for the cardioprotective effects of exercise in post-ischemic heart failure.International journal of cardiology. Heart & vasculature · 2025Article
- A comprehensive study on the impact ofFrontiers in cardiovascular medicine · 2025Article
- Protective effects of Dioscin against sepsis-induced cardiomyopathy via regulation of toll-like receptor 4/MyD88/p65 signal pathway.Immunity, inflammation and disease · 2024Article
- Berberine attenuates sepsis-induced cardiac dysfunction by upregulating the Akt/eNOS pathway in mice.Experimental and therapeutic medicine · 2022Article
- Ablation of cardiomyocyte-derived BDNF during development causes myocardial degeneration and heart failure in the adult mouse heart.Frontiers in cardiovascular medicine · 2022Article
- The regulatory role of the BDNF/TrkB pathway in organ and tissue fibrosis.Histology and histopathology · 2021Review
- Long non-coding RNA ZFAS1 alleviates sepsis-induced myocardial injury via target miR-34b-5p/SIRT1.Innate immunity · 2021Article
- Gastrodin alleviates inflammatory injury of cardiomyocytes in septic shock mice via inhibiting NLRP3 expression.In vitro cellular & developmental biology. Animal · 2021Article
- Interrelationships Between BDNF, Superoxide Dismutase, and Cognitive Impairment in Drug-Naive First-Episode Patients With Schizophrenia.Schizophrenia bulletin · 2020Article
- Involvement of neurotrophic signaling in doxorubicin-induced cardiotoxicity.Experimental and therapeutic medicine · 2020Article
- Article
- Upregulation of proBDNF in the Mesenteric Lymph Nodes in Septic Mice.Neurotoxicity research · 2019Article
- Obese mice exposed to psychosocial stress display cardiac and hippocampal dysfunction associated with local brain-derived neurotrophic factor depletion.EBioMedicine · 2019Article
- Roles of myokines in exercise-induced improvement of neuropsychiatric function.Pflugers Archiv : European journal of physiology · 2019Review
- An Integrative Review of Brain-Derived Neurotrophic Factor and Serious Cardiovascular Conditions.Nursing researchReview
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-induced myocardial dysfunction increases mortality in sepsis, yet the underlying mechanism is unclear. Brain-derived neurotrophic factor (BDNF) has been found to enhance cardiomyocyte function, but whether BDNF has a beneficial effect against septic myocardial dysfunction is unknown. Septic shock was induced by cecal ligation and puncture (CLP). BDNF was expressed in primary cardiomyocytes, and its expression was significantly reduced after sepsis. In rats with sepsis, a sharp decline in survival was observed after CLP, with significantly reduced cardiac BDNF expression, enhanced myocardial fibrosis, elevated oxidative stress, increased myocardial apoptosis, and decreased endothelial nitric oxide (NO) synthase (eNOS) and NO. Supplementation with recombined BDNF protein (rhBDNF) enhanced myocardial BDNF and increased survival rate with improved cardiac function, reduced oxidative stress, and myocardial apoptosis, which were associated with increased eNOS expression, NO production, and Trk-B, a BDNF receptor. Pretreatment with NOS inhibitor, N (omega)-nitro-L-arginine methyl ester, abolished the abovementioned BDNF cardioprotective effects without affecting BDNF and Trk-B. It is concluded that BDNF protects the heart against septic cardiac dysfunction by reducing oxidative stress and apoptosis via Trk-B, and it does so through activation of eNOS/NO pathway. These findings provide a new treatment strategy for sepsis-induced myocardial dysfunction.
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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.