ArticleCell communication and signaling : CCS2014
A p38MAPK/MK2 signaling pathway leading to redox stress, cell death and ischemia/reperfusion injury.
Article in Cell communication and signaling : CCS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed.
- 2,8-Dihydroxyquinoline ameliorates oligoasthenozoospermia by inhibiting MAPK14-mediated spermatogonial ferroptosis.Molecular biology reports · 2026Article
- Oxidative Stress in Health and Disease: Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Treadmill exercise activates mechanosensitive Piezo1 to inhibit cardiomyocyte apoptosis and improve cardiac function after myocardial infarction in mice.Basic research in cardiology · 2026Article
- MAPK14 converges on key transcriptional machinery to promote vascular smooth muscle cell degeneration in abdominal aortic aneurysm.Signal transduction and targeted therapy · 2026Article
- Artesunate preserves post-resuscitation myocardial and neurologic function in a rat model of cardiac arrest and cardiopulmonary resuscitation.Resuscitation plus · 2026Article
- Kv1.3 as an upstream regulator of oxidative stress-mediated neuroinflammation following organic dust exposure in murineFrontiers in toxicology · 2026Article
- Epigenetic downregulation of MAPKAPK2 exacerbates oxidative stress-induced damage in vitiligo melanocyte cell line model.Frontiers in medicine · 2026Article
- Qing-Xin-Jie-Yu granule prevents myocardial infarction-induced apoptosis via inhibition of p38 MAPK pathway.Frontiers in cardiovascular medicine · 2026Article
- Exercise Improves Heart Function after Myocardial Infarction: The Merits of AMPK.Cardiovascular drugs and therapy · 2025Review
- Protective effect and molecular mechanisms of magnolol in ischemic stroke.Pharmacological reports : PR · 2025Review
- The Redox Revolution in Brain Medicine: Targeting Oxidative Stress with AI, Multi-Omics and Mitochondrial Therapies for the Precision Eradication of Neurodegeneration.International journal of molecular sciences · 2025Review
- Jiao San Xian granule containing prebiotic alleviate functional dyspepsia by regulating intestinal flora and the secretion of inflammatory response.Journal of food and drug analysis · 2025Article
- Enhancing flu vaccine responses in older adults: preliminary insights from the ISOLDA study on immunosenescence and antioxidant and anti-inflammatory approaches.Immunity & ageing : I & A · 2025Article
- Increased oxidative phosphorylation through pyruvate dehydrogenase kinase 2 deficiency ameliorates cartilage degradation in mice with surgically induced osteoarthritis.Experimental & molecular medicine · 2025Article
- Biochanin-A: A Potential Candidate for the Treatment of Alzheimer's Disease.Current pharmaceutical biotechnology · 2025Review
- Identification of critical genes associated with oxidative stress pathways in benzene-induced hematotoxicity.Heliyon · 2024Article
- miR-124-3p downregulates EGR1 to suppress ischemia-hypoxia reperfusion injury in human iPS cell-derived cardiomyocytes.Scientific reports · 2024Article
- Identification of Drug Targets and Agents Associated with Ferroptosis-related Osteoporosis through Integrated Network Pharmacology and Molecular Docking Technology.Current pharmaceutical design · 2024Article
- An integral perspective of canonical cigarette and e-cigarette-related cardiovascular toxicity based on the adverse outcome pathway framework.Journal of advanced research · 2023Review
- The Potential Biotherapeutic Targets of Contrast-Induced Acute Kidney Injury.International journal of molecular sciences · 2023Review
4 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors.
Funding
Abstract
backgroundMany diseases and pathological conditions are characterized by transient or constitutive overproduction of reactive oxygen species (ROS). ROS are causal for ischemia/reperfusion (IR)-associated tissue injury (IRI), a major contributor to organ dysfunction or failure. Preventing IRI with antioxidants failed in the clinic, most likely due to the difficulty to timely and efficiently target them to the site of ROS production and action. IR is also characterized by changes in the activity of intracellular signaling molecules including the stress kinase p38MAPK. While ROS can cause the activation of p38MAPK, we recently obtained in vitro evidence that p38MAPK activation is responsible for elevated mitochondrial ROS levels, thus suggesting a role for p38MAPK upstream of ROS and their damaging effects.
resultsHere we identified p38MAPKα as the predominantly expressed isoform in HL-1 cardiomyocytes and siRNA-mediated knockdown demonstrated the pro-oxidant role of p38MAPKα signaling. Moreover, the knockout of the p38MAPK effector MAPKAP kinase 2 (MK2) reproduced the effect of inhibiting or knocking down p38MAPK. To translate these findings into a setting closer to the clinic a stringent kidney clamping model was used. p38MAPK activity increased upon reperfusion and p38MAPK inhibition by the inhibitor BIRB796 almost completely prevented severe functional impairment caused by IR. Histological and molecular analyses showed that protection resulted from decreased redox stress and apoptotic cell death.
conclusionsThese data highlight a novel and important mechanism for p38MAPK to cause IRI and suggest it as a potential therapeutic target for prevention of tissue injury.
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