ArticleInflammation2019
SS31 Ameliorates Sepsis-Induced Heart Injury by Inhibiting Oxidative Stress and Inflammation.
Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
30 citing papers in PubMed, 56 citations in OpenAlex.
- The central role of mitochondrial pathology in sepsis-induced cardiomyopathy: from molecular mechanisms to clinical translation.Frontiers in cardiovascular medicine · 2026Review
- PLK2 and the GSK3β-NRF2 Axis: A Promising Therapeutic Target for Sepsis-Induced Cardiac Injury?American journal of hypertension · 2025Article
- Predictive value of combined inflammatory markers for septic cardiomyopathy: a retrospective study.BMC infectious diseases · 2025Article
- Examination of mitochondria- and inflammasome-mediated mechanisms of clozapine-induced myocarditis using patient-derived iPSC cardiomyocytes.Molecular psychiatry · 2025Article
- Combatting sepsis-induced myocardial dysfunction: emerging mechanisms and immunomodulatory breakthroughs.Frontiers in immunology · 2025Review
- Study of the multitarget mechanism ofPharmaceutical biology · 2024Article
- Current Perspectives of Mitochondria in Sepsis-Induced Cardiomyopathy.International journal of molecular sciences · 2024Review
- Therapeutic Strategies Targeting Mitochondrial Dysfunction in Sepsis-induced Cardiomyopathy.Cardiovascular drugs and therapy · 2024Review
- Effect of L-carnitine in Ameliorating Lipopolysaccharide-Induced Cardiomyocyte Injury via MAPK Signaling.Molecular biotechnology · 2024Article
- Article
- SS31 Confers Cerebral Protection by Reversing Mitochondrial Dysfunction in Early Brain Injury Following Subarachnoid Hemorrhage, via the Nrf2- and PGC-1α-Dependent Pathways.Neurochemical research · 2023Article
- Mitochondrial transplantation protects against sepsis-induced myocardial dysfunction by modulating mitochondrial biogenesis and fission/fusion and inflammatory response.Molecular biology reports · 2023Article
- FOXO1 regulates NLRP3 inflammasome proteins in LPS-induced cardiotoxicity.American journal of translational research · 2023Article
- The Therapeutic Strategies Targeting Mitochondrial Metabolism in Cardiovascular Disease.Pharmaceutics · 2022Review
- The Interplay of Oxidative Stress and ROS Scavenging: Antioxidants as a Therapeutic Potential in Sepsis.Vaccines · 2022Review
- Berberine attenuates sepsis-induced cardiac dysfunction by upregulating the Akt/eNOS pathway in mice.Experimental and therapeutic medicine · 2022Article
- Article
- SS-31, a Mitochondria-Targeting Peptide, Ameliorates Kidney Disease.Oxidative medicine and cellular longevity · 2022Review
- Mitochondrial antioxidant SkQ1 decreases inflammation following hemorrhagic shock by protecting myocardial mitochondria.Frontiers in physiology · 2022Article
- β-Glucan from Saccharomyces cerevisiae alleviates oxidative stress in LPS-stimulated RAW264.7 cells via Dectin-1/Nrf2/HO-1 signaling pathway.Cell stress & chaperones · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Sepsis-induced myocardial dysfunction (SIMD), lack of effective treatment, accounts for high mortality of sepsis. Mitochondrion-targeted antioxidant peptide SS31 has been revealed to be responsible for certain cardiovascular disease by ameliorating oxidative stress injury. But whether it protects a septic heart remains little known. This study sought to prove that SS31 was capable of improving sepsis-induced myocardial dysfunction dramatically. C57BL/6 mice were intraperitoneally administered lipopolysaccharide (LPS), exposed to systemic inflammation. Thirty-five C57BL/6 mice were randomly divided into four groups: sham group, LPS group (5 mg/kg), SS31 group (5 mg/kg), and SS31 + LPS group (treatment group). Heart tissues were harvested for pathological examination at the indicated time points. H9C2 cell were treated with LPS with or without the presence of SS31 (10 μM) at 37 °C to assess the effect on cardiomyocytes at the indicated time points. SS31 restored myocardial morphological damage and suppressed inflammatory response as evidenced by significantly decreasing the mRNA levels of IL-6, IL-1β, and TNF-α in vitro and in vivo. In addition, myocardial energy deficiency secondary to sepsis was remarkedly ameliorated by SS31. Furthermore, we found that SS-31 normalized the activity of malondialdehyde, glutathione peroxidase, and superoxide dismutase in vitro and in vivo, and maintained mitochondrial membrane potential (MMP) as well. And western blot was applied to measure the expressions of p-p38MAPK, p-JNK1/2, p-ERK, p62, and NF-κB p65; the results illuminated that the cardioprotective effect of SS31 was partly linked to NF-κB. In conclusion, SS31 therapy effectively protected the heart against LPS-induced cardiac damage.
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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.