ArticleJournal of molecular and cellular cardiology2019
Acute AT
Article in Journal of molecular and cellular cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- Emerging Roles of Dystroglycan in Cardiac Remodeling, Fibrosis, and Heart Failure.International journal of molecular sciences · 2026Review
- Protection against isoproterenol-induced cardiac injury by sacubitril/valsartan is associated with upregulation of the alternative renin-angiotensin-aldosterone system pathway.Scientific reports · 2026Article
- Molecular Mechanisms and Therapeutic Strategies in Heart Failure Due to Dystrophin Deficiency: A Comprehensive Review.Reviews in cardiovascular medicine · 2026Review
- AAV-microutrophin gene therapy confers durable cardioprotection against pharmacologic and exercise-induced injury in the mdx mouse.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Friend or Foe?: The Immune System's Dilemma With Dystrophin Replacement Therapy.JACC. Basic to translational science · 2025Article
- DG9 boosts PMO nuclear uptake and exon skipping to restore dystrophic muscle and cardiac function.Nature communications · 2025Article
- Qingda Granule Attenuates Hypertension-Induced Cardiac Damage via Regulating Renin-Angiotensin System Pathway.Chinese journal of integrative medicine · 2025Article
- Klotho Is Cardioprotective in the mdx Mouse Model of Duchenne Muscular Dystrophy.The American journal of pathology · 2025Article
- Functional cardiac consequences of β-adrenergic stress-induced injury in a model of Duchenne muscular dystrophy.Disease models & mechanisms · 2024Article
- Physiological stress improves stem cell modeling of dystrophic cardiomyopathy.Disease models & mechanisms · 2024Article
- Reduced cardiac antioxidant defenses mediate increased susceptibility to workload-induced myocardial injury in males with genetic cardiomyopathy.Journal of molecular and cellular cardiology · 2024Article
- Functional cardiac consequences of β-adrenergic stress-induced injury in thebioRxiv : the preprint server for biology · 2024Article
- Mechanisms of reduced myocardial energetics of the dystrophic heart.American journal of physiology. Heart and circulatory physiology · 2024Article
- Role of cAMP in Cardiomyocyte Viability: Beneficial or Detrimental?Circulation research · 2023Article
- Molecular homing and retention of muscle membrane stabilizing copolymers by non-invasive optical imaging in vivo.Molecular therapy. Methods & clinical development · 2023Article
- Storax Attenuates Cardiac Fibrosis following Acute Myocardial Infarction in Rats via Suppression of AT1R-Ankrd1-P53 Signaling Pathway.International journal of molecular sciences · 2022Article
- Cardioprotective effect of nicorandil on isoproterenol induced cardiomyopathy in the Mdx mouse model.BMC cardiovascular disorders · 2021Article
- The cardioprotective effect of the sodium-glucose cotransporter 2 inhibitor dapagliflozin in rats with isoproterenol-induced cardiomyopathy.American journal of translational research · 2021Article
- Role of the Renin-Angiotensin-Aldosterone System in Dystrophin-Deficient Cardiomyopathy.International journal of molecular sciences · 2020Review
- Social stress is lethal in the mdx model of Duchenne muscular dystrophy.EBioMedicine · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundDuchenne muscular dystrophy (DMD) is an X-linked disease characterized by skeletal muscle degeneration and a significant cardiomyopathy secondary to cardiomyocyte damage and myocardial loss. The molecular basis of DMD lies in the absence of the protein dystrophin, which plays critical roles in mechanical membrane integrity and protein localization at the sarcolemma. A popular mouse model of DMD is the mdx mouse, which lacks dystrophin and displays mild cardiac and skeletal pathology that can be exacerbated to advance the disease state. In clinical and pre-clinical studies of DMD, angiotensin signaling pathways have emerged as therapeutic targets due to their adverse influence on muscle remodeling and oxidative stress. Here we aim to establish a physiologically relevant cardiac injury model in the mdx mouse, and determine whether acute blockade of the angiotensin II type 1 receptor (AT METHODS AND
resultsA single IP injection of isoproterenol (Iso, 10 mg/kg) was used to induce cardiac stress and injury in mdx and wild type (C57Bl/10) mice. Mice were euthanized 8 h, 30 h, 1 week, or 1 month following the injection, and hearts were harvested for injury evaluation. At 8 and 30 h post-injury, mdx hearts showed 2.2-fold greater serum cTnI content and 3-fold more extensive injury than wild type hearts. Analysis of hearts 1 week and 1 month after injury revealed significantly higher fibrosis in mdx hearts, with a more robust and longer-lasting immune response compared to wild type hearts. In the 30-hour group, losartan treatment initiated 1 h before Iso injection protected dystrophic hearts from cardiac damage, reducing mdx acute injury area by 2.8-fold, without any significant effect on injury in wild type hearts. However, both wild type and dystrophic hearts showed a 2-fold reduction in the magnitude of the macrophage response to injury 30 h after Iso with losartan.
conclusionsThis work demonstrates that acute blockade of AT
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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.