ArticleProceedings of the National Academy of Sciences of the United States of America2015
Endothelin-1 critically influences cardiac function via superoxide-MMP9 cascade.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
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- Circulatory Maternal Endothelin 1 and Matrix Metalloproteinase-9 Gene Expression in PREECLAMPSIA: A Study in Western Uttar Pradesh, India.Journal of obstetrics and gynaecology of India · 2023Article
- Could Endothelin-1 Be a Promising Neurohormonal Biomarker in Acute Heart Failure?Diagnostics (Basel, Switzerland) · 2023Review
- Circulating biomarkers for management of cancer therapeutics-related cardiac dysfunction.Cardiovascular research · 2023Review
- Big Endothelin-1 as a Predictor of Reverse Remodeling and Prognosis in Dilated Cardiomyopathy.Journal of clinical medicine · 2023Article
- Modeling incomplete penetrance in arrhythmogenic cardiomyopathy by human induced pluripotent stem cell derived cardiomyocytes.Computational and structural biotechnology journal · 2023Article
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- Integrated bioinformatic analysis reveals immune molecular markers and potential drugs for diabetic cardiomyopathy.Frontiers in endocrinology · 2022Article
- Interplay of cardiovascular mediators, oxidative stress and inflammation in liver disease and its complications.Nature reviews. Cardiology · 2021Review
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- Endothelin-1, cardiac morphology, and heart failure: the MESA angiogenesis study.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2020Article
- New Insights and Current Approaches in Cardiac Hypertrophy Cell Culture, Tissue Engineering Models, and Novel Pathways Involving Non-Coding RNA.Frontiers in pharmacology · 2020Review
- Article
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
We have generated low-expressing and high-expressing endothelin-1 genes (L and H) and have bred mice with four levels of expression: L/L, ∼20%; L/+, ∼65%; +/+ (wild type), 100%; and H/+, ∼350%. The hypomorphic L allele can be spatiotemporally switched to the hypermorphic H allele by Cre-loxP recombination. Young adult L/L and L/+ mice have dilated cardiomyopathy, hypertension, and increased plasma volumes, together with increased ventricular superoxide levels, increased matrix metalloproteinase 9 (Mmp9) expression, and reduced ventricular stiffness. H/+ mice have decreased plasma volumes and significantly heavy stiff hearts. Global or cardiomyocyte-specific switching expression from L to H normalized the abnormalities already present in young adult L/L mice. An epithelial sodium channel antagonist normalized plasma volume and blood pressure, but only partially corrected the cardiomyopathy. A superoxide dismutase mimetic made superoxide levels subnormal, reduced Mmp9 overexpression, and substantially improved cardiac function. Genetic absence of Mmp9 also improved cardiac function, but increased superoxide remained. We conclude that endothelin-1 is critical for maintaining normal contractile function, for controlling superoxide and Mmp9 levels, and for ensuring that the myocardium has sufficient collagen to prevent overstretching. Even a modest (∼35%) decrease in endothelin-1 gene (Edn1) expression is sufficient to cause cardiac dysfunction.
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Registered trials
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