Chronic heart failure: Ca2+, catabolism, and catastrophic cell death

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

卷:1862

Review

Cho, Geoffrey W.¹  Altamirano, Francisco¹  Hill, Joseph A.^1,2 

[1] Univ Texas SW Med Ctr Dallas, Dept Internal Med Cardiol, Dallas, TX 75390 USA

[2] Univ Texas SW Med Ctr Dallas, Dept Mol Biol, Dallas, TX 75390 USA

关键词: Heart failure;    Remodeling;    Calcium homeostasis;    Autophagy;    Apoptosis;   

DOI  :  10.1016/j.bbadis.2016.01.011

来源: Elsevier

【 摘 要 】

Robust successes have been achieved in recent years in conquering the acutely lethal manifestations of heart disease. Many patients who previously would have died now survive to enjoy happy and productive lives. Nevertheless, the devastating impact of heart disease continues unabated, as the spectrum of disease has evolved with new manifestations. In light of this ever-evolving challenge, insights that culminate in novel therapeutic targets are urgently needed. Here, we review fundamental mechanisms of heart failure, both with reduced (HFrEF) and preserved (HFpEF) ejection fraction. We discuss pathways that regulate cardiomyocyte remodeling and turnover, focusing on Ca2+ signaling, autophagy, and apoptosis. In particular, we highlight recent insights pointing to novel connections among these events. We also explore mechanisms whereby potential therapeutic approaches targeting these processes may improve morbidity and mortality in the devastating syndrome of heart failure. (C) 2016 Elsevier B.V. All rights reserved.

【 授权许可】

Free