ReviewPflugers Archiv : European journal of physiology2011
Role of autocrine/paracrine mechanisms in response to myocardial strain.
Review in Pflugers Archiv : European journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 59 citations in OpenAlex.
- Exercise-induced cardiac mitochondrial reorganization and enhancement in spontaneously hypertensive rats.Pflugers Archiv : European journal of physiology · 2024Article
- Differential sensitivity to longitudinal and transverse stretch mediates transcriptional responses in mouse neonatal ventricular myocytes.American journal of physiology. Heart and circulatory physiology · 2024Article
- Secretoneurin as a Novel Biomarker of Cardiovascular Episodes: Are We There Yet? A Narrative Review.Journal of clinical medicine · 2022Review
- iTRAQ‑based quantitative proteomics analysis of the potential application of secretoneurin gene therapy for cardiac hypertrophy induced by DL‑isoproterenol hydrochloride in mice.International journal of molecular medicine · 2020Article
- Stretch-Induced Biased Signaling in Angiotensin II Type 1 and Apelin Receptors for the Mediation of Cardiac Contractility and Hypertrophy.Frontiers in physiology · 2020Review
- Control of cardiac contraction by sodium: Promises, reckonings, and new beginnings.Cell calcium · 2020Review
- TRPC3 participates in angiotensin II type 1 receptor-dependent stress-induced slow increase in intracellular CaThe journal of physiological sciences : JPS · 2018Article
- Physiologic, Pathologic, and Therapeutic Paracrine Modulation of Cardiac Excitation-Contraction Coupling.Circulation research · 2018Review
- Impact of titin strain on the cardiac slow force response.Progress in biophysics and molecular biology · 2017Article
- Cardiac inotropy, lusitropy, and CaPflugers Archiv : European journal of physiology · 2016Article
- Acute Myocardial Response to Stretch: What We (don't) Know.Frontiers in physiology · 2015Review
- Endogenous endothelin 1 mediates angiotensin II-induced hypertrophy in electrically paced cardiac myocytes through EGFR transactivation, reactive oxygen species and NHE-1.Pflugers Archiv : European journal of physiology · 2014Article
- Novel approaches to determine contractile function of the isolated adult zebrafish ventricular cardiac myocyte.The Journal of physiology · 2014Article
- The autocrine/paracrine loop after myocardial stretch: mineralocorticoid receptor activation.Current cardiology reviews · 2013Review
- The role of the paracrine/autocrine mediator endothelin-1 in regulation of cardiac contractility and growth.British journal of pharmacology · 2013Review
- Mitochondrial reactive oxygen species (ROS) as signaling molecules of intracellular pathways triggered by the cardiac renin-angiotensin II-aldosterone system (RAAS).Frontiers in physiology · 2013Article
- Intermedin suppresses pressure overload cardiac hypertrophy through activation of autophagy.PloS one · 2013Article
- Inhibition of Na⁺-H⁺ exchange as a mechanism of rapid cardioprotection by resveratrol.British journal of pharmacology · 2012Article
- Mineralocorticoid receptor activation is crucial in the signalling pathway leading to the Anrep effect.The Journal of physiology · 2011Article
- In vivo key role of reactive oxygen species and NHE-1 activation in determining excessive cardiac hypertrophy.Pflugers Archiv : European journal of physiology · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial strain triggers an autocrine/paracrine mechanism known to participate in myocardial hypertrophy development. After the onset of stretch, there is a rapid augmentation in developed tension due to an increase in myofilament calcium sensitivity (the Frank Starling mechanism) followed by a gradual increase in tension over the next 10-15 min. This second phase is called the slow force response (SFR) to stretch and is known to be the result of an increase in calcium transient amplitude. In the present review, we will discuss what is known thus far about the SFR, which is the in vitro equivalent of the Anrep effect and the mechanical counterpart of the autocrine/paracrine mechanism elicited by myocardial stretch. The chain of events triggered by myocardial stretch comprises: (1) release of angiotensin II, (2) release/formation of endothelin, (3) NADPH oxidase activation and transactivation of the EGFR, (4) mitochondrial reactive oxygen species production, (5) activation of redox-sensitive kinases, (6) NHE-1 hyperactivity, (7) increase in intracellular Na(+) concentration, and (8) increase in Ca(2+) transient amplitude through the Na(+)/Ca(2+) exchanger. The evidence for each step of the intracellular signaling pathway leading to the development of SFR and their relationship with the mechanisms proposed for cardiac hypertrophy development will be analyzed.
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