ArticleHuman molecular genetics2019
Mineralocorticoid receptor antagonists improve membrane integrity independent of muscle force in muscular dystrophy.
Article in Human molecular genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Defining the potential role of the mineralocorticoid receptor in musculoskeletal health and bone crosstalk with other tissues.The Journal of endocrinology · 2026Review
- Direct aldosterone stimulation of skeletal muscle fibroblasts changes gene expression and differentially affects fibroblast functions from normal and diseased muscles.Frontiers in physiology · 2026Article
- Mineralocorticoid receptor antagonists reduce inflammatory signaling independent of myofiber mineralocorticoid receptor.Endocrine and metabolic science · 2025Article
- Intercellular communication from myotubes to fibroblasts is differentially impacted by mineralocorticoid receptor signaling and muscular dystrophy.Cell communication and signaling : CCS · 2025Article
- Physiological stress improves stem cell modeling of dystrophic cardiomyopathy.Disease models & mechanisms · 2024Article
- Cell-type specific effects of mineralocorticoid receptor gene expression suggest intercellular communication regulating fibrosis in skeletal muscle disease.Frontiers in physiology · 2024Article
- Micro-dystrophin gene therapy demonstrates long-term cardiac efficacy in a severe Duchenne muscular dystrophy model.Molecular therapy. Methods & clinical development · 2023Article
- Mineralocorticoid receptor antagonists and glucocorticoids differentially affect skeletal muscle inflammation and pathology in muscular dystrophy.JCI insight · 2022Article
- Myeloid mineralocorticoid receptors contribute to skeletal muscle repair in muscular dystrophy and acute muscle injury.American journal of physiology. Cell physiology · 2022Article
- Mineralocorticoid Receptor Signaling in the Inflammatory Skeletal Muscle Microenvironments of Muscular Dystrophy and Acute Injury.Frontiers in pharmacology · 2022Review
- Muscle Twitch Kinetics Are Dependent on Muscle Group, Disease State, and Age in Duchenne Muscular Dystrophy Mouse Models.Frontiers in physiology · 2020Article
- Mineralocorticoid Receptor Signaling Contributes to Normal Muscle Repair After Acute Injury.Frontiers in physiology · 2019Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Mineralocorticoid receptor (MR) drugs have been used clinically for decades to treat cardiovascular diseases. MR antagonists not only show preclinical efficacy for heart in Duchenne muscular dystrophy (DMD) models but also improve skeletal muscle force and muscle membrane integrity. The mechanisms of action of MR antagonists in skeletal muscles are entirely unknown. Since MR are present in many cell types in the muscle microenvironment, it is critical to define cell-intrinsic functions in each cell type to ultimately optimize antagonist efficacy for use in the widest variety of diseases. We generated a new conditional knockout of MR in myofibers and quantified cell-intrinsic mechanistic effects on functional and histological parameters in a DMD mouse model. Skeletal muscle MR deficiency led to improved respiratory muscle force generation and less deleterious fibrosis but did not reproduce MR antagonist efficacy on membrane susceptibility to induced damage. Surprisingly, acute application of MR antagonist to muscles led to improvements in membrane integrity after injury independent of myofiber MR. These data demonstrate that MR antagonists are efficacious to dystrophic skeletal muscles through both myofiber intrinsic effects on muscle force and downstream fibrosis and extrinsic functions on membrane stability. MR antagonists may therefore be applicable for treating more general muscle weakness and possibly other conditions that result from cell injuries.
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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.