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Changes in T-Tubules and Sarcoplasmic Reticulum in Ventricular Myocytes in Early Cardiac Hypertrophy in a Pressure Overload Rat Model
Author(s) -
Perla Pérez-Treviño,
Jorge Pérez-Treviño,
Cuauhtémoc Borja-Villa,
Noemı́ Garcı́a,
Julio Altamirano
Publication year - 2015
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000430254
Subject(s) - medicine , muscle hypertrophy , myocyte , pressure overload , contractility , endoplasmic reticulum , endocrinology , heart failure , fluorescence recovery after photobleaching , chemistry , biology , microbiology and biotechnology , cardiac hypertrophy , biochemistry , membrane
Pressure-overload (PO) causes cardiac hypertrophy (CH), and eventually leads to heart failure (HF). HF ventricular myocytes present transverse-tubules (TT) loss or disarrangement and decreased sarcoplasmic reticulum (SR) density, and both contribute to altered Ca2+ signaling and heart dysfunction. It has been shown that TT remodeling precedes HF, however, it is unknown whether SR structural and functional remodeling also starts early in CH.

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