ArticleJournal of translational medicine2023
Angiotensin-(1-7) ameliorates sepsis-induced cardiomyopathy by alleviating inflammatory response and mitochondrial damage through the NF-κB and MAPK pathways.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- PINK1-Parkin pathway-mediated mitophagy in sepsis: friend or foe?Molecular biology reports · 2026Review
- Recombinant myonectin ameliorates sepsis‑induced cardiomyopathy by alleviating mitochondrial dysfunction via the AdipoR1/AMPK pathway.International journal of molecular medicine · 2026Article
- Mas receptor activation regulates the functional phenotype of myocardial macrophages through the Akt/Nrf2 signaling pathway to alleviate sepsis-induced cardiomyopathy.Journal of translational medicine · 2026Article
- Role of oxidative stress in sepsis: Mechanisms, pathways, and therapeutic strategies.Journal of pharmaceutical analysis · 2026Review
- Taurine Alleviates Sepsis-Induced Myocardial Injury by Inhibiting NF-κB Pathway-Mediated Inflammation, Mitochondrial Dysfunction, and Apoptosis.Cardiovascular toxicology · 2026Article
- Frontiers in the diagnosis and treatment of sepsis-induced cardiomyopathy: current status and prospects.Frontiers in cardiovascular medicine · 2026Review
- Therapeutical progress in sepsis-induced cardiomyopathy.Frontiers in cardiovascular medicine · 2026Review
- Mitochondrial dysfunction in mesenchymal stem cells impairs osteogenesis in radiation-induced bone injury via CaCell death & disease · 2025Article
- Sepsis-Related Cardiomyopathy: Advances in Diagnosis and Treatment.Reviews in cardiovascular medicine · 2025Review
- HIPK2 Confers Protection Against Septic Myocardial Injury by Regulating Ferroptosis.Cardiovascular toxicology · 2025Article
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- Mitochondria at the Heart of Sepsis: Mechanisms, Metabolism, and Sex Differences.International journal of molecular sciences · 2025Review
- Sepsis-induced cardiomyopathy: understanding pathophysiology and clinical implications.Archives of toxicology · 2025Review
- Polysaccharides of Atractylodes Macrocephala Koidz Alleviate LPS-Induced Bursa of Fabricius Injury in Goslings by Inhibiting EREG Expression.Animals : an open access journal from MDPI · 2025Article
- Angiotensin-(1-7) protective effects in neurocognitive disorders: molecular mechanisms to therapeutic implications.Frontiers in physiology · 2025Review
- Activation of central Angiotensin-(1-7)/Mas receptor alleviates synaptic damage in diabetes-associated cognitive impairment via modulating AKT/FOXO1/PACAP axis.International journal of biological sciences · 2025Article
- Establishment of a Novel in vitro Model of Sepsis-Induced Myocardial Injury Using Septic Serum: A Comprehensive Comparative Study.Journal of inflammation research · 2025Article
- Advancements in macrophage research for cardiovascular disease.Frontiers in physiology · 2025Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThere is no available viable treatment for Sepsis-Induced Cardiomyopathy (SIC), a common sepsis complication with a higher fatality risk. The septic patients showed an abnormal activation of the renin angiotensin (Ang) aldosterone system (RAAS). However, it is not known how the Ang II and Ang-(1-7) affect SIC.
methodsPeripheral plasma was collected from the Healthy Control (HC) and septic patients and Ang II and Ang-(1-7) protein concentrations were measured. The in vitro and in vivo models of SIC were developed using Lipopolysaccharide (LPS) to preliminarily explore the relationship between the SIC state, Ang II, and Ang-(1-7) levels, along with the protective function of exogenous Ang-(1-7) on SIC.
resultsPeripheral plasma Ang II and the Ang II/Ang-(1-7) levels in SIC-affected patients were elevated compared to the levels in HC and non-SIC patients, however, the HC showed higher Ang-(1-7) levels. Furthermore, peripheral plasma Ang II, Ang II/Ang-(1-7), and Ang-(1-7) levels in SIC patients were significantly correlated with the degree of myocardial injury. Additionally, exogenous Ang-(1-7) can attenuate inflammatory response, reduce oxidative stress, maintain mitochondrial dynamics homeostasis, and alleviate mitochondrial structural and functional damage by inhibiting nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways, thus alleviating SIC.
conclusionsPlasma Ang-(1-7), Ang II, and Ang II/Ang-(1-7) levels were regarded as significant SIC biomarkers. In SIC, therapeutic targeting of RAAS, for example with Ang-(1-7), may exert protective roles against myocardial damage.
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