Matrix elasticity regulates the optimal cardiac myocyte shape for contractility
نویسندگان
چکیده
منابع مشابه
Matrix elasticity regulates the optimal cardiac myocyte shape for contractility.
Concentric hypertrophy is characterized by ventricular wall thickening, fibrosis, and decreased myocyte length-to-width aspect ratio. Ventricular thickening is considered compensatory because it reduces wall stress, but the functional consequences of cell shape remodeling in this pathological setting are unknown. We hypothesized that decreases in myocyte aspect ratio allow myocytes to maximize ...
متن کاملMyocyte shape regulates lateral registry of sarcomeres and contractility.
The heart actively remodels architecture in response to various physiological and pathological conditions. Gross structural change of the heart chambers is directly reflected at the cellular level by altering the morphological characteristics of individual cardiomyocytes. However, an understanding of the relationship between cardiomyocyte shape and the contractile function remains unclear. By u...
متن کاملKChIP2 regulates the cardiac Ca2+ transient and myocyte contractility by targeting ryanodine receptor activity
Pathologic electrical remodeling and attenuated cardiac contractility are featured characteristics of heart failure. Coinciding with these remodeling events is a loss of the K+ channel interacting protein, KChIP2. While, KChIP2 enhances the expression and stability of the Kv4 family of potassium channels, leading to a more pronounced transient outward K+ current, Ito,f, the guinea pig myocardiu...
متن کاملMitochondrial matrix metalloproteinase activation decreases myocyte contractility in hyperhomocysteinemia.
Cardiomyocyte N-methyl-d-aspartate receptor-1 (NMDA-R1) activation induces mitochondrial dysfunction. Matrix metalloproteinase protease (MMP) induction is a negative regulator of mitochondrial function. Elevated levels of homocysteine [hyperhomocysteinemia (HHCY)] activate latent MMPs and causes myocardial contractile abnormalities. HHCY is associated with mitochondrial dysfunction. We tested t...
متن کاملCardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function.
RATIONALE Fatty acid oxidation is transcriptionally regulated by peroxisome proliferator-activated receptor (PPAR)α and under normal conditions accounts for 70% of cardiac ATP content. Reduced Ppara expression during sepsis and heart failure leads to reduced fatty acid oxidation and myocardial energy deficiency. Many of the transcriptional regulators of Ppara are unknown. OBJECTIVE To determi...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: American Journal of Physiology-Heart and Circulatory Physiology
سال: 2014
ISSN: 0363-6135,1522-1539
DOI: 10.1152/ajpheart.00799.2013