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Source: Cellular Signalling
Condition: Heart Failure

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Total 7 results found since Jan 2013.

SGK1 is necessary to FoxO3a negative regulation, oxidative stress and cardiac fibroblast activation induced by TGF- β1
Cell Signal. 2023 Jun 19;109:110778. doi: 10.1016/j.cellsig.2023.110778. Online ahead of print.ABSTRACTCardiac fibroblasts (CFs) activation is a common response to most pathological conditions affecting the heart, characterized by increased cellular secretory capacity and increased expression of fibrotic markers, such as collagen I and smooth muscle actin type alpha (α-SMA). Fibrotic activation of CFs induces the increase in tissue protein content, with the consequent tissue stiffness, diastolic dysfunction, and heart failure. Therefore, the search for new mechanisms of CFs activation is important to find novel treatments...
Source: Cellular Signalling - June 21, 2023 Category: Cytology Authors: Fabiola Gonz ález-Herrera Mabel Catal án Renatto Anfossi Juan Diego Maya Zully Pedrozo Guillermo D íaz-Araya Ra úl Vivar Source Type: research

RhoA regulates Drp1 mediated mitochondrial fission through ROCK to protect cardiomyocytes.
Abstract Cardiac ischemia/reperfusion, loss of blood flow and its subsequent restoration, causes damage to the heart. Oxidative stress from ischemia/reperfusion leads to dysfunction and death of cardiomyocytes, increasing the risk of progression to heart failure. Alterations in mitochondrial dynamics, in particular mitochondrial fission, have been suggested to play a role in cardioprotection from oxidative stress. We tested the hypothesis that activation of RhoA regulates mitochondrial fission in cardiomyocytes. Our studies show that expression of constitutively active RhoA in cardiomyocytes increases phosphorylat...
Source: Cellular Signalling - June 25, 2018 Category: Cytology Authors: Brand CS, Tan VP, Brown JH, Miyamoto S Tags: Cell Signal Source Type: research

Regulation of cellular oxidative stress and apoptosis by G protein-coupled receptor kinase-2; The role of NADPH oxidase 4.
Abstract Cardiac myocyte oxidative stress and apoptosis are considered important mechanisms for the development of heart failure (HF). Chronic HF is characterized by increased circulating catecholamines to augment cardiac output. Long-term stimulation of myocardial β-adrenergic receptors (β-ARs) is deleterious in cardiac myocytes, however, the potential mechanisms underlying increased cell death are unclear. We hypothesize that GRK2, a critical regulator of myocardial β-AR signaling, plays an important role in mediating cellular oxidative stress and apoptotic cell death in response to β-agonist stimulation. St...
Source: Cellular Signalling - November 26, 2015 Category: Cytology Authors: Theccanat T, Philip JL, Razzaque A, Ludmer N, Li J, Xu X, Akhter SA Tags: Cell Signal Source Type: research

Small interfering RNA therapy against carbohydrate sulfotransferase 15 inhibits cardiac remodeling in rats with dilated cardiomyopathy.
Abstract Carbohydrate sulfotransferase 15 (CHST15) is a sulfotransferase responsible for biosynthesis of chondroitin sulfate E (CS-E), which plays important roles in numerous biological events such as biosynthesis of proinflammatory cytokines. However, the effects of CHST15 siRNA in rats with chronic heart failure (CHF) after experimental autoimmune myocarditis (EAM) have not yet been investigated. CHF was elicited in Lewis rats by immunization with cardiac myosin, and after immunization, the rats were divided into two groups and treated with either CHST15 siRNA (2μg/week) or vehicle. Age matched normal rats with...
Source: Cellular Signalling - March 14, 2015 Category: Cytology Authors: Watanabe K, Arumugam S, Sreedhar R, Thandavarayan RA, Nakamura T, Nakamura M, Harima M, Yoneyama H, Suzuki K Tags: Cell Signal Source Type: research