ArticleHuman molecular genetics2017
Androgen receptor agonists increase lean mass, improve cardiopulmonary functions and extend survival in preclinical models of Duchenne muscular dystrophy.
Article in Human molecular genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Chronic inflammation as a driving factor for sarcopenia: an update on pathophysiology and future therapeutic targets.Frontiers in pharmacology · 2026Review
- Are we giving too much weight to lean mass loss?Molecular metabolism · 2025Review
- Ligandrol lowers endurance and negatively affects lipid and hormonal profile of male rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Neurology of Androgens and Androgenic Supplements.Current neurology and neuroscience reports · 2025Review
- A molecular switch from tumor suppressor to oncogene in ER+ve breast cancer: Role of androgen receptor, JAK-STAT, and lineage plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A rapid synthesis of molecularly imprinted polymer nanoparticles for the extraction of performance enhancing drugs (PIEDs).Nanoscale advances · 2023Article
- Identification and Synthesis of Selected In Vitro Generated Metabolites of the Novel Selective Androgen Receptor Modulator (SARM) 2f.Molecules (Basel, Switzerland) · 2023Article
- Selective Androgen Receptor Modulators: An Emerging Liver Toxin.Journal of clinical and translational hepatology · 2023Review
- Androgen receptor regulates the proliferation of myoblasts under appropriate or excessive stretch through IGF-1 receptor mediated p38 and ERK1/2 pathways.Nutrition & metabolism · 2021Article
- Catalpol counteracts the pathology in a mouse model of Duchenne muscular dystrophy by inhibiting the TGF-β1/TAK1 signaling pathway.Acta pharmacologica Sinica · 2021Article
- Lack of miR-378 attenuates muscular dystrophy in mdx mice.JCI insight · 2020Article
- Selective androgen receptor modulators: the future of androgen therapy?Translational andrology and urology · 2020Review
- Crucial role of androgen receptor in resistance and endurance trainings-induced muscle hypertrophy through IGF-1/IGF-1R- PI3K/Akt- mTOR pathway.Nutrition & metabolism · 2020Article
- Androgen Receptor Is a Non-canonical Inhibitor of Wild-Type and Mutant Estrogen Receptors in Hormone Receptor-Positive Breast Cancers.iScience · 2019Article
- Hits Discovery on the Androgen Receptor: In Silico Approaches to Identify Agonist Compounds.Cells · 2019Article
- Normalizing Plasma Renin Activity in Experimental Dilated Cardiomyopathy: Effects on Edema, Cachexia, and Survival.International journal of molecular sciences · 2019Article
- Selective Androgen Receptor Modulators: Current Knowledge and Clinical Applications.Sexual medicine reviews · 2019Review
- Targeting the Muscle-Bone Unit: Filling Two Needs with One Deed in the Treatment of Duchenne Muscular Dystrophy.Current osteoporosis reports · 2018Review
- Skeletal Muscle Pathophysiology: The Emerging Role of Spermine Oxidase and Spermidine.Medical sciences (Basel, Switzerland) · 2018Review
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a neuromuscular disease that predominantly affects boys as a result of mutation(s) in the dystrophin gene. DMD is characterized by musculoskeletal and cardiopulmonary complications, resulting in shorter life-span. Boys afflicted by DMD typically exhibit symptoms within 3-5 years of age and declining physical functions before attaining puberty. We hypothesized that rapidly deteriorating health of pre-pubertal boys with DMD could be due to diminished anabolic actions of androgens in muscle, and that intervention with an androgen receptor (AR) agonist will reverse musculoskeletal complications and extend survival. While castration of dystrophin and utrophin double mutant (mdx-dm) mice to mimic pre-pubertal nadir androgen condition resulted in premature death, maintenance of androgen levels extended the survival. Non-steroidal selective-AR modulator, GTx-026, which selectively builds muscle and bone was tested in X-linked muscular dystrophy mice (mdx). GTx-026 significantly increased body weight, lean mass and grip strength by 60-80% over vehicle-treated mdx mice. While vehicle-treated castrated mdx mice exhibited cardiopulmonary impairment and fibrosis of heart and lungs, GTx-026 returned cardiopulmonary function and intensity of fibrosis to healthy control levels. GTx-026 elicits its musculoskeletal effects through pathways that are distinct from dystrophin-regulated pathways, making AR agonists ideal candidates for combination approaches. While castration of mdx-dm mice resulted in weaker muscle and shorter survival, GTx-026 treatment increased the muscle mass, function and survival, indicating that androgens are important for extended survival. These preclinical results support the importance of androgens and the need for intervention with AR agonists to treat DMD-affected boys.
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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.