ArticleFrontiers in pharmacology2021
Physical Activity and Inhibition of ACE Additively Modulate ACE/ACE-2 Balance in Heart Failure in Mice.
Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Liver sinusoidal endothelial cell defenestration in chronic heart failure is primarily dependent on cardiac diastolic dysfunction and is reversed by a sodium-glucose cotransporter 2 inhibitor but not by an angiotensin-converting enzyme inhibitor.Cardiovascular research · 2026Article
- Changes in Physical Activity Following Heart Failure in Humans and Animal Models: A Scoping Review.Current heart failure reports · 2026Review
- Defects in auxiliary fuel oxidation and mitochondrial pyruvate transport mark transition to overt heart failure in Tgαq*44 mice.Journal of translational medicine · 2026Article
- Physical activity of moderate-intensity optimizes myocardial citrate cycle in a murine model of heart failure.Frontiers in physiology · 2025Article
- Respiratory issues in patients with multiple sclerosis as a risk factor during SARS-CoV-2 infection: a potential role for exercise.Molecular and cellular biochemistry · 2023Review
- Moderate Intensity Aerobic Exercise Potential Favorable Effect Against COVID-19: The Role of Renin-Angiotensin System and Immunomodulatory Effects.Frontiers in physiology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiotensin-converting enzyme inhibition (ACE-I) and physical activity favorably modulate the ACE/ACE-2 balance. However, it is not clear whether physical activity and ACE-I could synergistically modulate ACE/ACE-2 balance in the course of heart failure (HF). Here, we studied the effects of combined spontaneous physical activity and ACE-I-based treatment on angiotensin (Ang) pattern and cardiac function in a mouse model of HF (Tgαq*44). Tgαq*44 mice with advanced HF (at the age of 12 months) were running spontaneously in a running wheel (exercise training group, ExT) and/or were treated with ACE inhibitor (ACE-I, perindopril, 10 mg/kg) for 2 months. Angiotensin profile was characterized by an LC-MS/MS-based method. The cardiac performance was assessed
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