ArticlePloS one2014
ACE2 is augmented in dystrophic skeletal muscle and plays a role in decreasing associated fibrosis.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- The role of COVID-19 in myopathy: incidence, causes, treatment, and prevention.Journal of medicine and life · 2022Pooled it
- Molecular mechanisms of skeletal muscle fibrosis and potential targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Therapeutic Efficacy of HPβ-CD-Angiotensin-(1-7) Oral Formulation in Muscle Injury Recovery in Rat.Journal of cellular and molecular medicine · 2025Article
- Graphene Oxide Decreases Pro-Inflammatory Proteins Production in Skeletal Muscle Cells Exposed to SARS-CoV-2 Spike Protein.Nanotechnology, science and applications · 2023Article
- Muscle dysfunction in the long coronavirus disease 2019 syndrome: Pathogenesis and clinical approach.Reviews in medical virology · 2022Review
- Virtual Screening of Natural Chemical Databases to Search for Potential ACE2 Inhibitors.Molecules (Basel, Switzerland) · 2022Article
- Serum Sestrin-1 Concentration Is Higher in Frail than Non-Frail Older People Living in Nursing Homes.International journal of environmental research and public health · 2022Article
- Speculation on the pathophysiology of musculoskeletal injury with COVID-19 infection.Frontiers in medicine · 2022Article
- Osteosarcopenia and Long-COVID: a dangerous combination.Therapeutic advances in musculoskeletal disease · 2022Review
- The Musculoskeletal Involvement After Mild to Moderate COVID-19 Infection.Frontiers in physiology · 2022Review
- Unraveling Muscle Impairment Associated With COVID-19 and the Role of 3D Culture in Its Investigation.Frontiers in nutrition · 2022Review
- Angiotensin 1-7 prevents the excessive force loss resulting from 14- and 28-day denervation in mouse EDL and soleus muscle.The Journal of general physiology · 2021Article
- Article
- Moderate exercise may prevent the development of severe forms of COVID-19, whereas high-intensity exercise may result in the opposite.Medical hypotheses · 2021Article
- Ang-(1-7) protects skeletal muscle function in aged mice.BMC musculoskeletal disorders · 2021Article
- CoQ10 augments candesartan protective effect against tourniquet-induced hind limb ischemia-reperfusion: Involvement of non-classical RAS and ROS pathways.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2021Article
- Hyperactivated RAGE in Comorbidities as a Risk Factor for Severe COVID-19-The Role of RAGE-RAS Crosstalk.Biomolecules · 2021Review
- Multinational Prevalence of Neurological Phenotypes in Patients Hospitalized with COVID-19.medRxiv : the preprint server for health sciences · 2021Article
- Pain during and after coronavirus disease 2019: Chinese perspectives.Pain reports · 2021Review
- ACE2, angiotensin 1-7 and skeletal muscle: review in the era of COVID-19.Clinical science (London, England : 1979) · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is the most common inherited neuromuscular disease and is characterized by absence of the cytoskeletal protein dystrophin, muscle wasting, and fibrosis. We previously demonstrated that systemic infusion or oral administration of angiotensin-(1-7) (Ang-(1-7)), a peptide with opposing effects to angiotensin II, normalized skeletal muscle architecture, decreased local fibrosis, and improved muscle function in mdx mice, a dystrophic model for DMD. In this study, we investigated the presence, activity, and localization of ACE2, the enzyme responsible for Ang-(1-7) production, in wild type (wt) and mdx skeletal muscle and in a model of induced chronic damage in wt mice. All dystrophic muscles studied showed higher ACE2 activity than wt muscle. Immunolocalization studies indicated that ACE2 was localized mainly at the sarcolemma and, to a lesser extent, associated with interstitial cells. Similar results were observed in the model of chronic damage in the tibialis anterior (TA) muscle. Furthermore, we evaluated the effect of ACE2 overexpression in mdx TA muscle using an adenovirus containing human ACE2 sequence and showed that expression of ACE2 reduced the fibrosis associated with TA dystrophic muscles. Moreover, we observed fewer inflammatory cells infiltrating the mdx muscle. Finally, mdx gastrocnemius muscles from mice infused with Ang-(1-7), which decreases fibrosis, contain less ACE2 associated with the muscle. This is the first evidence supporting ACE2 as an important therapeutic target to improve the dystrophic skeletal muscle phenotype.
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