ArticleJournal of applied physiology (Bethesda, Md. : 1985)2015
AT1 receptor blocker losartan protects against mechanical ventilation-induced diaphragmatic dysfunction.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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
23 citing papers in PubMed, 32 citations in OpenAlex.
- Ventilator-induced diaphragmatic dysfunction: pathophysiology, monitoring and advances in potential treatment and prevention.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Angiotensin II Type 1 Receptor Blocker Usage Prevents Oxidative Stress and Muscle Dysfunction in HIV.Fundamental & clinical pharmacology · 2025Article
- Diaphragm Function in Health and Disease.Advances in experimental medicine and biology · 2025Review
- Research progress on the pathogenesis and treatment of ventilator-induced diaphragm dysfunction.Heliyon · 2023Review
- Losartan treatment attenuates hindlimb unloading-induced atrophy in the soleus muscle of female rats via canonical TGF-β signaling.The journal of physiological sciences : JPS · 2022Article
- Alterations in renin-angiotensin receptors are not responsible for exercise preconditioning of skeletal muscle fibers.Sports medicine and health science · 2021Article
- Angiotensin 1-7 protects against ventilator-induced diaphragm dysfunction.Clinical and translational science · 2021Article
- Role of Matricellular CCN Proteins in Skeletal Muscle: Focus on CCN2/CTGF and Its Regulation by Vasoactive Peptides.International journal of molecular sciences · 2021Review
- Comparative Efficacy of Angiotensin II Type 1 Receptor Blockers Against Ventilator-Induced Diaphragm Dysfunction in Rats.Clinical and translational science · 2021Article
- SARS-CoV-2/Renin-Angiotensin System: Deciphering the Clues for a Couple with Potentially Harmful Effects on Skeletal Muscle.International journal of molecular sciences · 2020Review
- Redox Control of Proteolysis During Inactivity-Induced Skeletal Muscle Atrophy.Antioxidants & redox signaling · 2020Review
- Article
- Disturbances in Calcium Homeostasis Promotes Skeletal Muscle Atrophy: Lessons From Ventilator-Induced Diaphragm Wasting.Frontiers in physiology · 2020Review
- Muscle wasting: A review of exercise, classical and non-classical RAS axes.Journal of cellular and molecular medicine · 2019Review
- The regulation of skeletal muscle fatigability and mitochondrial function by chronically elevated interleukin-6.Experimental physiology · 2019Article
- Angiotensin-(1-7) exerts a protective action in a rat model of ventilator-induced diaphragmatic dysfunction.Intensive care medicine experimental · 2019Article
- Increased SOD2 in the diaphragm contributes to exercise-induced protection against ventilator-induced diaphragm dysfunction.Redox biology · 2019Article
- The Renin-Angiotensin System and Skeletal Muscle.Exercise and sport sciences reviews · 2018Review
- Increased skeletal muscle mitochondrial free radical production in peripheral arterial disease despite preserved mitochondrial respiratory capacity.Experimental physiology · 2018Article
- Smad3 initiates oxidative stress and proteolysis that underlies diaphragm dysfunction during mechanical ventilation.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Mechanical ventilation is a life-saving intervention for patients in respiratory failure. Unfortunately, prolonged ventilator support results in diaphragmatic atrophy and contractile dysfunction leading to diaphragm weakness, which is predicted to contribute to problems in weaning patients from the ventilator. While it is established that ventilator-induced oxidative stress is required for the development of ventilator-induced diaphragm weakness, the signaling pathway(s) that trigger oxidant production remain unknown. However, recent evidence reveals that increased plasma levels of angiotensin II (ANG II) result in oxidative stress and atrophy in limb skeletal muscles. Using a well-established animal model of mechanical ventilation, we tested the hypothesis that increased circulating levels of ANG II are required for both ventilator-induced diaphragmatic oxidative stress and diaphragm weakness. Cause and effect was determined by administering an angiotensin-converting enzyme inhibitor (enalapril) to prevent ventilator-induced increases in plasma ANG II levels, and the ANG II type 1 receptor antagonist (losartan) was provided to prevent the activation of ANG II type 1 receptors. Enalapril prevented the increase in plasma ANG II levels but did not protect against ventilator-induced diaphragmatic oxidative stress or diaphragm weakness. In contrast, losartan attenuated both ventilator-induced oxidative stress and diaphragm weakness. These findings indicate that circulating ANG II is not essential for the development of ventilator-induced diaphragm weakness but that activation of ANG II type 1 receptors appears to be a requirement for ventilator-induced diaphragm weakness. Importantly, these experiments provide the first evidence that the Food and Drug Administration-approved drug losartan may have clinical benefits to protect against ventilator-induced diaphragm weakness in humans.
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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.