ArticlePloS one2009
Losartan decreases p42/44 MAPK signaling and preserves LZ+ MYPT1 expression.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Aging related decreases in NM myosin expression and contractility in a resistance vessel.Frontiers in physiology · 2024Article
- Role of Angiotensin II in Cardiovascular Diseases: Introducing Bisartans as a Novel Therapy for Coronavirus 2019.Biomolecules · 2023Review
- Angiotensin II type 1 receptor blockade attenuates gefitinib-induced cardiac hypertrophy via adjusting angiotensin II-mediated oxidative stress and JNK/P38 MAPK pathway in a rat model.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022Article
- The vasculature in HFpEF vs HFrEF: differences in contractile protein expression produce distinct phenotypes.Heliyon · 2020Article
- Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders.Pharmacological reviews · 2016Review
- MYPT1 isoforms expressed in HEK293T cells are differentially phosphorylated after GTPγS treatment.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2016Article
- Angiotensin II inhibits satellite cell proliferation and prevents skeletal muscle regeneration.The Journal of biological chemistry · 2013Article
- Altered reactivity of tertiary mesenteric arteries following acute myocardial ischemia.Journal of vascular research · 2013Article
- Losartan restores skeletal muscle remodeling and protects against disuse atrophy in sarcopenia.Science translational medicine · 2011Article
- Pleiotropic effects of angiotensin receptor blockers: addressing comorbidities by optimizing hypertension therapy.Journal of clinical hypertension (Greenwich, Conn.) · 2011Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Heart failure is associated with impairment in nitric oxide (NO) mediated vasodilatation, which has been demonstrated to result from a reduction in the relative expression of the leucine zipper positive (LZ+) isoform of the myosin targeting subunit (MYPT1) of myosin light chain phosphatase. Further, captopril preserves normal LZ+ MYPT1 expression, the sensitivity to cGMP-mediated vasodilatation and modulates the expression of genes in the p42/44 MAPK and p38 MAPK signaling cascades. This study tests whether angiotensin receptor blockade (ARB) with losartan decreases p42/44 MAPK or p38 MAPK signaling and preserves LZ+ MYPT1 expression in a rat infarct model of heart failure. In aortic smooth muscle, p42/44 MAPK activation increases and LZ+ MYPT1 expression falls after LAD ligation. Losartan treatment decreases the activation of p42/44 MAPK to the uninfarcted control level and preserves normal LZ+ MYPT1 expression. The expression and activation of p38 MAPK, however, is low and does not change following LAD ligation or with losartan therapy. These data suggest that either reducing or blocking the effects of circulating angiotensin II, both decreases the activation of the p42/44 MAPK signaling cascade and preserves LZ+ MYPT1 expression. Thus, the ability of ACE-inhibitors and ARBs to modulate the vascular phenotype, to preserve normal flow mediated vasodilatation may explain the beneficial effects of these drugs compared to other forms of afterload reduction in the treatment of heart failure.
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