ArticleJournal of molecular and cellular cardiology2014
Mitochondria-targeted ROS scavenger improves post-ischemic recovery of cardiac function and attenuates mitochondrial abnormalities in aged rats.
Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 87 citations in OpenAlex.
- Mitochondrial remodeling in heart failure with reduced ejection fraction.Frontiers in physiology · 2026Review
- Mitochondrial alterations induced by Macrovipera lebetina venom.European biophysics journal : EBJ · 2025Article
- Targeting Mitochondrial Reactive Oxygen Species: JP4-039's Potential as a Cardiovascular Therapeutic.Journal of clinical medicine · 2025Review
- Nitroxides: Chemistry, Antioxidant Properties, and Biomedical Applications.Molecules (Basel, Switzerland) · 2025Review
- Mechanisms of postischemic cardiac death and protection following myocardial injury.The Journal of clinical investigation · 2025Review
- Oxidative stress and its related epigenetic modifications in vascular calcification: mechanisms and advances.Frontiers in cardiovascular medicine · 2025Review
- Article
- Role of AMPK and Sirtuins in Aging Heart: Basic and Translational Aspects.Aging and disease · 2024Review
- Redox-active vitamin C suppresses human osteosarcoma growth by triggering intracellular ROS-iron-calcium signaling crosstalk and mitochondrial dysfunction.Redox biology · 2024Article
- GPR50 regulates neuronal development as a mitophagy receptor.Cell death & disease · 2024Article
- Cellular ROS and Antioxidants: Physiological and Pathological Role.Antioxidants (Basel, Switzerland) · 2024Article
- Intrinsic and Extrinsic Contributors to the Cardiac Benefits of Exercise.JACC. Basic to translational science · 2024Review
- Ferroptosis mechanisms and regulations in cardiovascular diseases in the past, present, and future.Cell biology and toxicology · 2024Review
- XJB-5-131 protects chondrocytes from ferroptosis to alleviate osteoarthritis progression via restoring Pebp1 expression.Journal of orthopaedic translation · 2024Article
- Mitochondrial Calcium Overload Plays a Causal Role in Oxidative Stress in the Failing Heart.Biomolecules · 2023Review
- Does treatment with autophagy-enhancers and/or ROS-scavengers alleviate behavioral and neurochemical consequences of low-dose rotenone-induced mild mitochondrial dysfunction in mice?Molecular psychiatry · 2023Article
- Reduction in mitochondrial ROS improves oxidative phosphorylation and provides resilience to coronary endothelium in non-reperfused myocardial infarction.Basic research in cardiology · 2023Article
- Effects of Ferroptosis on the Metabolome in Cardiac Cells: The Role of Glutaminolysis.Antioxidants (Basel, Switzerland) · 2022Article
- The Role of Probiotics in Skin Photoaging and Related Mechanisms: A Review.Clinical, cosmetic and investigational dermatology · 2022Review
- HDAC4 Inhibitors as Antivascular Senescence Therapeutics.Oxidative medicine and cellular longevity · 2022Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Mitochondria-generated reactive oxygen species (ROS) play a crucial role in the pathogenesis of aging and age-associated diseases. In this study, we evaluated the effects of XJB-5-131 (XJB), a mitochondria-targeted ROS and electron scavenger, on cardiac resistance to ischemia-reperfusion (IR)-induced oxidative stress in aged rats. Male adult (5-month old, n=17) and aged (29-month old, n=19) Fischer Brown Norway (F344/BN) rats were randomly assigned to the following groups: adult (A), adult+XJB (AX), aged (O), and aged+XJB (OX). XJB was administered 3 times per week (3mg/kg body weight, IP) for four weeks. At the end of the treatment period, cardiac function was continuously monitored in excised hearts using the Langendorff technique for 30 min, followed by 20 min of global ischemia, and 60-min reperfusion. XJB improved post-ischemic recovery of aged hearts, as evidenced by greater left ventricular developed-pressures and rate-pressure products than the untreated, aged-matched group. The state 3 respiration rates at complexes I, II and IV of mitochondria isolated from XJB-treated aged hearts were 57% (P<0.05), 25% (P<0.05) and 28% (P<0.05), respectively, higher than controls. Ca(2+)-induced swelling, an indicator of permeability transition pore opening, was reduced in the mitochondria of XJB-treated aged rats. In addition, XJB significantly attenuated the H2O2-induced depolarization of the mitochondrial inner membrane as well as the total and mitochondrial ROS levels in cultured cardiomyocytes. This study underlines the importance of mitochondrial ROS in aging-induced cardiac dysfunction and suggests that targeting mitochondrial ROS may be an effective therapeutic approach to protect the aged heart against IR injury.
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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.