Chronic heart failure

Ca2+, catabolism, and catastrophic cell death

Geoffrey W. Cho, Francisco Altamirano, Joseph A Hill

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)763-777
Number of pages15
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
Volume1862
Issue number4
DOIs
StatePublished - Apr 1 2016

Fingerprint

Heart Diseases
Cell Death
Heart Failure
Autophagy
Cardiac Myocytes
Apoptosis
Morbidity
Mortality
Therapeutics

Keywords

  • Apoptosis
  • Autophagy
  • Calcium homeostasis
  • Heart failure
  • Remodeling

ASJC Scopus subject areas

  • Molecular Biology
  • Molecular Medicine

Cite this

Chronic heart failure : Ca2+, catabolism, and catastrophic cell death. / Cho, Geoffrey W.; Altamirano, Francisco; Hill, Joseph A.

In: Biochimica et Biophysica Acta - Molecular Basis of Disease, Vol. 1862, No. 4, 01.04.2016, p. 763-777.

Research output: Contribution to journalArticle

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