ArticleJournal of cellular physiology2018
Blunting of estrogen modulation of cardiac cellular chymase/RAS activity and function in SHR.
Article in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Estrogen depletion modulates aortic prothrombotic signaling in normotensive and spontaneously hypertensive female rats.Molecular and cellular endocrinology · 2023Article
- Sex differences in the renin-angiotensin-aldosterone system and its roles in hypertension, cardiovascular, and kidney diseases.Frontiers in cardiovascular medicine · 2023Review
- Heart Failure in Menopause: Treatment and New Approaches.International journal of molecular sciences · 2022Review
- The renin-angiotensin system biomolecular cascade: a 2022 update of newer insights and concepts.Kidney international supplements · 2022Review
- Is Sex a Determinant of COVID-19 Infection? Truth or Myth?Current hypertension reports · 2020Review
- Noncanonical Mechanisms for Direct Bone Marrow Generating Ang II (Angiotensin II) Predominate in CD68 Positive Myeloid Lineage Cells.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Estrogen modulates the differential expression of cardiac myocyte chymase isoforms and diastolic function.Molecular and cellular biochemistry · 2019Article
- Activation of the Human Angiotensin-(1-12)-Chymase Pathway in Rats With Human Angiotensinogen Gene Transcripts.Frontiers in cardiovascular medicine · 2019Article
- G protein-coupled estrogen receptor (GPER) deficiency induces cardiac remodeling through oxidative stress.Translational research : the journal of laboratory and clinical medicine · 2018Article
- Critical role of the chymase/angiotensin-(1-12) axis in modulating cardiomyocyte contractility.International journal of cardiology · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The relatively low efficacy of ACE-inhibitors in the treatment of heart failure in women after estrogen loss may be due to their inability to reach the intracellular sites at which angiotensin (Ang) II is generated and/or the existence of cell-specific mechanisms in which ACE is not the essential processing pathway for Ang II formation. We compared the metabolic pathway for Ang II formation in freshly isolated myocytes (CMs) and non-myocytes (NCMs) in cardiac membranes extracted from hearts of gonadal-intact and ovariectomized (OVX) adult WKY and SHR rats. Plasma Ang II levels were higher in WKY vs. SHR (strain effect: WKY: 62 ± 6 pg/ml vs. SHR: 42 ± 9 pg/ml; p < 0.01), independent of OVX. The enzymatic activities of chymase, ACE, and ACE2 were higher in NCMs versus CMs, irrespective of whether assays were performed in cardiac membranes from WKY or SHR or in the presence or absence of OVX. E2 depletion increased chymase activity, but not ACE activity, in both CMs and NCMs. Moreover, cardiac myocyte chymase activity associated with diastolic function in WKYs and cardiac structure in SHRs while no relevant functional and structural relationships between the classic enzymatic pathway of Ang II formation by ACE or the counter-regulatory Ang-(1-7) forming path from Ang II via ACE2 were apparent. The significance of these novel findings is that targeted cell-specific chymase rather than ACE inhibition may have a greater benefit in the management of HF in women after menopause.
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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 Socratic graph.