Key result
Enhanced activity of the cardiac Na+/H+ exchanger (NHE-1) after myocardial stretch acts as a key early signal for the development of cardiac hypertrophy, which can be regressed by specific NHE-1 blockade.
Highlights the theoretical mechanistic role of NHE-1 and subsequent Ca2+ signaling in the development of stretch-induced cardiac hypertrophy.
NHE-1 blockade may regress stretch-induced hypertrophy; leaves open clinical translation pending trials.
The enhanced activity of the cardiac Na+/H+ exchanger (NHE-1) after myocardial stretch is considered a key step of the intracellular signaling pathway leading to the slow force response to stretch as well as an early signal for the development of cardiac hypertrophy. We propose that the chain of events triggered by stretch begins with the release of small amounts of Angiotensin II (Ang II)/endothelin (ET) and ends with the increase in intracellular Ca2+ concentration ([Ca2+]i) through the Na+/Ca2+ exchanger in reverse mode (NCX(rev)), which triggers cardiac hypertrophy by activation of widely recognized Ca2+-dependent intracellular signaling pathways.
No takes yet. Share an insight, caveat, or question.
E. Cingolani Horacio (2008) conducted a review in Cardiac hypertrophy. NHE-1 blockade was evaluated. Enhanced activity of the cardiac Na+/H+ exchanger (NHE-1) after myocardial stretch acts as a key early signal for the development of cardiac hypertrophy, which can be regressed by specific NHE-1 blockade.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: