ArticleHuman molecular genetics2016
Myeloid cells are capable of synthesizing aldosterone to exacerbate damage in muscular dystrophy.
Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03777319 (A Randomized Open Label Trial of Spironolactone Versus Prednisolone in Corticosteroid-naïve Boys With DMD), which is not on this map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Randomized Open Label Trial of Spironolactone Versus Prednisolone in Corticosteroid-naïve Boys With DMD
Who cites it
22 citing papers in PubMed, 20 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
- Targeting nuclear receptors in muscular dystrophies and regenerative myogenesis.Frontiers in cell and developmental biology · 2026Review
- 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
- Regulatory role of vitamin DScientific reports · 2025Article
- Cell-type specific effects of mineralocorticoid receptor gene expression suggest intercellular communication regulating fibrosis in skeletal muscle disease.Frontiers in physiology · 2024Article
- Mineralocorticoid receptor antagonists and glucocorticoids differentially affect skeletal muscle inflammation and pathology in muscular dystrophy.JCI insight · 2022Article
- Immune modulatory effects of progesterone on oxLDL-induced trained immunity in monocytes.Journal of leukocyte biology · 2022Article
- Myeloid mineralocorticoid receptors contribute to skeletal muscle repair in muscular dystrophy and acute muscle injury.American journal of physiology. Cell physiology · 2022Article
- Immune Cells as Critical Regulators of Steroidogenesis in the Testis and Beyond.Frontiers in endocrinology · 2022Review
- Mineralocorticoid Receptor Signaling in the Inflammatory Skeletal Muscle Microenvironments of Muscular Dystrophy and Acute Injury.Frontiers in pharmacology · 2022Review
- Decreased Glucocorticoid Signaling Potentiates Lipid-Induced Inflammation and Contributes to Insulin Resistance in the Skeletal Muscle of Fructose-Fed Male Rats Exposed to Stress.International journal of molecular sciences · 2021Article
- To Curb the Progression of Fatal COVID-19 Course-Dream or Reality.Current hypertension reports · 2021Review
- Sodium-induced inflammation-an invisible player in resistant hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Review
- Cardiac Pathophysiology and the Future of Cardiac Therapies in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2019Review
- Mineralocorticoid receptor antagonists improve membrane integrity independent of muscle force in muscular dystrophy.Human molecular genetics · 2019Article
- Acute ATJournal of molecular and cellular cardiology · 2019Article
- Vamorolone targets dual nuclear receptors to treat inflammation and dystrophic cardiomyopathy.Life science alliance · 2019Article
- 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
8 authors at 3 institutions in 1 country.
Funding
Abstract
FDA-approved mineralocorticoid receptor (MR) antagonists are used to treat heart failure. We have recently demonstrated efficacy of MR antagonists for skeletal muscles in addition to heart in Duchenne muscular dystrophy mouse models and that mineralocorticoid receptors are present and functional in skeletal muscles. The goal of this study was to elucidate the underlying mechanisms of MR antagonist efficacy on dystrophic skeletal muscles. We demonstrate for the first time that infiltrating myeloid cells clustered in damaged areas of dystrophic skeletal muscles have the capacity to produce the natural ligand of MR, aldosterone, which in excess is known to exacerbate tissue damage. Aldosterone synthase protein levels are increased in leukocytes isolated from dystrophic muscles compared with controls and local aldosterone levels in dystrophic skeletal muscles are increased, despite normal circulating levels. All genes encoding enzymes in the pathway for aldosterone synthesis are expressed in muscle-derived leukocytes. 11β-HSD2, the enzyme that inactivates glucocorticoids to increase MR selectivity for aldosterone, is also increased in dystrophic muscle tissues. These results, together with the demonstrated preclinical efficacy of antagonists, suggest MR activation is in excess of physiological need and likely contributes to the pathology of muscular dystrophy. This study provides new mechanistic insight into the known contribution of myeloid cells to muscular dystrophy pathology. This first report of myeloid cells having the capacity to produce aldosterone may have implications for a wide variety of acute injuries and chronic diseases with inflammation where MR antagonists may be therapeutic.
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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.