ArticleCell death & disease2020
Pyroptosis and ferroptosis induced by mixed lineage kinase 3 (MLK3) signaling in cardiomyocytes are essential for myocardial fibrosis in response to pressure overload.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed, 216 citations in OpenAlex.
- Ferroptosis: Newly Emerged Regulator for Human Disease.MedComm · 2026Review
- Molecular mechanisms of iron metabolism and ferroptosis in cardiovascular diseases and intervention strategies targeting natural products (Review).Molecular medicine reports · 2026Review
- Potential Relationship Between Ferroptosis and Pyroptosis in Myocardial Ischemia/Reperfusion Injury: Molecular Mechanisms and Therapeutic Targets.Reviews in cardiovascular medicine · 2026Review
- MLK3 promotes atherosclerosis by regulating ferroptosis in macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Hydroxytyrosol attenuates obesity-induced myocardial fibrosis by inhibiting NLRP3/CYLD/NOX4 mediated oxidative stress.NPJ science of food · 2026Article
- Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- TARDBP Mediates the MAP3K11/SLC3A2/GPX4 Axis in Alzheimer's Disease Rats by Enhancing KRAS mRNA Stability.Journal of cellular and molecular medicine · 2026Article
- Thymoquinone Protects Against Cardiac Hypertrophy via PPAR-γ/PI3K/Akt Pathway.Journal of cellular and molecular medicine · 2026Article
- Inhibition of Setd7 protects against cardiomyocyte hypertrophy via inhibiting lipid oxidation.Acta pharmacologica Sinica · 2026Article
- Nonpolysaccharide fraction ofFrontiers in pharmacology · 2026Article
- The Regulatory Landscape of Ferroptosis and Iron Homeostasis: Pathophysiological Mechanisms and Therapeutic Horizons in Cardiovascular Disease.Drug design, development and therapy · 2026Review
- The role of different types of programmed cell death in myocardial fibrosis: from mechanisms to therapeutics.Frontiers in cardiovascular medicine · 2026Review
- α-Linolenic Acid Alleviates Diabetic Cardiomyopathy by Activating AMPK-STAT3 Pathway to Inhibit Ferritinophagy and Enhance SLC7A11-GPX4 Antioxidant Axis.Molecules (Basel, Switzerland) · 2025Article
- Mixed lineage kinase 3 contributes to myocardial ischemia/reperfusion injury by regulating neutrophil activation.Basic research in cardiology · 2025Article
- Targeting pyroptosis in myocardial inflammation and fibrosis: molecular mechanisms and therapeutic strategies.Apoptosis : an international journal on programmed cell death · 2025Review
- Research progress on programmed cell death of cardiomyocytes in pressure-overload hypertrophic cardiomyopathy.Apoptosis : an international journal on programmed cell death · 2025Review
- 4-Methylesculetin alleviated aflatoxin B1-induced liver injury and ferritinophagy through AMPK- TOR-Ulk axis in grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2025Article
- CD36 attenuates pressure overload-induced myocardial insulin resistance via HSF1-dependent HSP90α suppression and competitive disruption of the HSP90α-InsR complex.Journal of translational medicine · 2025Article
- The role of JNK signaling pathway in organ fibrosis.Journal of advanced research · 2025Review
- The Trim32-DPEP2 axis is an inflammatory switch in macrophages during intestinal inflammation.Cell death and differentiation · 2025Article
48 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic heart failure (CHF) is the final outcome of many cardiovascular diseases, and is a severe health issue faced by the elderly population. Mixed lineage kinase 3 (MLK3), a member of MAP3K family, is associated with aging, inflammation, oxidative stress, and related diseases, such as CHF. MLK3 has also been reported to play an important role in protecting against cardiomyocyte injury; however, its function in myocardial fibrosis is unknown. To investigate the role of MLK3 in myocardial fibrosis, we inhibited the expression of MLK3, and examined cardiac function and remodeling in TAC mice. In addition, we assessed the expression of MLK3 protein in ventricular cells and its downstream associated protein. We found that MLK3 mainly regulates NF-κB/NLRP3 signaling pathway-mediated inflammation and that pyroptosis causes myocardial fibrosis in the early stages of CHF. Similarly, MLK3 mainly regulates the JNK/p53 signaling pathway-mediated oxidative stress and that ferroptosis causes myocardial fibrosis in the advanced stages of CHF. We also found that promoting the expression of miR-351 can inhibit the expression of MLK3, and significantly improve cardiac function in mice subjected to TAC. These results suggest the pyroptosis and ferroptosis induced by MLK3 signaling in cardiomyocytes are essential for adverse myocardial fibrosis, in response to pressure overload. Furthermore, miR-351, which has a protective effect on ventricular remodeling in heart failure caused by pressure overload, may be a key target for the regulation of MLK3.
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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.