ArticleClinical science (London, England : 1979)2014
Chronic oral administration of Ang-(1-7) improves skeletal muscle, autonomic and locomotor phenotypes in muscular dystrophy.
Article in Clinical science (London, England : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- Therapeutic Efficacy of HPβ-CD-Angiotensin-(1-7) Oral Formulation in Muscle Injury Recovery in Rat.Journal of cellular and molecular medicine · 2025Article
- One Copy Number Variation within the Angiopoietin-1 Gene Is Associated with Leizhou Black Goat Meat Quality.Animals : an open access journal from MDPI · 2024Article
- Unraveling Muscle Impairment Associated With COVID-19 and the Role of 3D Culture in Its Investigation.Frontiers in nutrition · 2022Review
- Ang-(1-7) protects skeletal muscle function in aged mice.BMC musculoskeletal disorders · 2021Article
- Role of the Renin-Angiotensin-Aldosterone System in Dystrophin-Deficient Cardiomyopathy.International journal of molecular sciences · 2020Review
- ACE2, angiotensin 1-7 and skeletal muscle: review in the era of COVID-19.Clinical science (London, England : 1979) · 2020Review
- Fibrogenesis inFrontiers in molecular neuroscience · 2020Review
- Muscle wasting: A review of exercise, classical and non-classical RAS axes.Journal of cellular and molecular medicine · 2019Review
- Activating Mas receptor protects human pulmonary microvascular endothelial cells against LPS-induced apoptosis via the NF-kB p65/P53 feedback pathways.Journal of cellular physiology · 2019Article
- Mas Receptor Activation Slows Tumor Growth and Attenuates Muscle Wasting in Cancer.Cancer research · 2019Article
- Angiotensin-(1-7) exerts a protective action in a rat model of ventilator-induced diaphragmatic dysfunction.Intensive care medicine experimental · 2019Article
- Combined Therapies for Duchenne Muscular Dystrophy to Optimize Treatment Efficacy.Frontiers in genetics · 2018Review
- The ACE2/Angiotensin-(1-7)/MAS Axis of the Renin-Angiotensin System: Focus on Angiotensin-(1-7).Physiological reviews · 2018Review
- Significance of angiotensin 1-7 coupling with MAS1 receptor and other GPCRs to the renin-angiotensin system: IUPHAR Review 22.British journal of pharmacology · 2017Review
- Article
- New agents modulating the renin-angiotensin-aldosterone system-Will there be a new therapeutic option?Experimental biology and medicine (Maywood, N.J.) · 2016Review
- Myocardial Contractile Dysfunction Is Present without Histopathology in a Mouse Model of Limb-Girdle Muscular Dystrophy-2F and Is Prevented after Claudin-5 Virotherapy.Frontiers in physiology · 2016Article
- The angiotensin-(1-7)/Mas axis reduces myonuclear apoptosis during recovery from angiotensin II-induced skeletal muscle atrophy in mice.Pflugers Archiv : European journal of physiology · 2015Article
- Angiotensin-dependent autonomic dysregulation precedes dilated cardiomyopathy in a mouse model of muscular dystrophy.Experimental physiology · 2015Article
- Expression of the Mas receptor is upregulated in skeletal muscle wasting.Histochemistry and cell biology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Muscular dystrophies are a group of heterogeneous genetic disorders that cause progressive muscle weakness and wasting, dilated cardiomyopathy and early mortality. There are different types of muscular dystrophies with varying aetiologies but they all have a common hallmark of myofibre degeneration, atrophy and decreased mobility. Mutation in Sgcd (sarcoglycan-δ), a subunit of dystrophin glycoprotein complex, causes LGMD2F (limb girdle muscular dystrophy 2F). Previously, we have reported that Sgcd-deficient (Sgcd-/-) mice exhibit AngII (angiotensin II)-induced autonomic and skeletal muscle dysfunction at a young age, which contributes to onset of dilated cardiomyopathy and mortality at older ages. Two counter-regulatory RAS (renin-angiotensin system) pathways have been identified: deleterious actions of AngII acting on the AT1R (AngII type 1 receptor) compared with the protective actions of Ang-(1-7) [angiotensin-(1-7)] acting on the receptor Mas. We propose that the balance between the AngII/AT1R and Ang-(1-7)/Mas axes is disturbed in Sgcd-/- mice. Control C57BL/6J and Sgcd-/- mice were treated with Ang-(1-7) included in hydroxypropyl β-cyclodextrin (in drinking water) for 8-9 weeks beginning at 3 weeks of age. Ang-(1-7) treatment restored the AngII/AT1R compared with Ang-(1-7)/Mas balance, decreased oxidative stress and fibrosis in skeletal muscle, increased locomotor activity, and prevented autonomic dysfunction without lowering blood pressure in Sgcd-/- mice. Our results suggest that correcting the early autonomic dysregulation by administering Ang-(1-7) or enhancing its endogenous production may provide a novel therapeutic approach in muscular dystrophy.
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Registered trials
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