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International journal of molecular sciences
Jul 09, 2021;22 (14):

Calcium and Heart Failure: How Did We Get Here and Where Are We Going?

Natthaphat Siri-Angkul, Behzad Dadfar, Riya Jaleel, Jazna Naushad, Jaseela Parambathazhath, Angelia A Doye, Lai-Hua Xie, Judith K Gwathmey
Author Information
  1. Natthaphat Siri-Angkul: Department of Cell Biology and Molecular Medicine, Rutgers University-New Jersey Medical School, Newark, NJ 07103, USA.
  2. Behzad Dadfar: Department of General Medicine, School of Medicine, Mazandaran University of Medical Sciences, Sari 1471655836, Iran. ORCID
  3. Riya Jaleel: School of International Education, Zhengzhou University, Zhengzhou 450001, China. ORCID
  4. Jazna Naushad: Weill Cornell Medicine Qatar, Doha P. O. Box 24144, Qatar.
  5. Jaseela Parambathazhath: Process Dynamics Laboratories, Al Khor 679576, Qatar.
  6. Angelia A Doye: Gwathmey Inc., Cambridge, MA 02138, USA.
  7. Lai-Hua Xie: Department of Cell Biology and Molecular Medicine, Rutgers University-New Jersey Medical School, Newark, NJ 07103, USA.
  8. Judith K Gwathmey: Department of Cell Biology and Molecular Medicine, Rutgers University-New Jersey Medical School, Newark, NJ 07103, USA.
PMID: 34299010 DOI: 10.3390/ijms22147392

Abstract

The occurrence and prevalence of heart failure remain high in the United States as well as globally. One person dies every 30 s from heart disease. Recognizing the importance of heart failure, clinicians and scientists have sought better therapeutic strategies and even cures for end-stage heart failure. This exploration has resulted in many failed clinical trials testing novel classes of pharmaceutical drugs and even gene therapy. As a result, along the way, there have been paradigm shifts toward and away from differing therapeutic approaches. The continued prevalence of death from heart failure, however, clearly demonstrates that the heart is not simply a pump and instead forces us to consider the complexity of simplicity in the pathophysiology of heart failure and reinforces the need to discover new therapeutic approaches.

Keywords

beta blocker calcium transient excitation–contraction coupling heart failure hypoxia inotrope myocardial contractility myofilament sarcoplasmic reticulum sarcoplasmic reticulum Ca2+ ATPase

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Grants

  1. R01HL49574; R01HL49574; R01HL39091; R01HL97979; R01HL133294/NIH HHS
  2. R01 HL157116/NHLBI NIH HHS
  3. R01 HL133294/NHLBI NIH HHS
  4. PMAYP/Prince Mahidol Award Foundation, Thailand
  5. 19TPA34900003/American Heart Association

MeSH Term

Adenosine Triphosphatases
Adrenergic beta-1 Receptor Agonists
Adrenergic beta-Antagonists
Animals
Antioxidants
Ca(2+) Mg(2+)-ATPase
Calcium
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Cardiotonic Agents
Dobutamine
Heart Failure
Humans
Myocardial Contraction
Sarcoplasmic Reticulum

Chemicals

Adrenergic beta-1 Receptor Agonists
Adrenergic beta-Antagonists
Antioxidants
Cardiotonic Agents
Dobutamine
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Adenosine Triphosphatases
Ca(2+) Mg(2+)-ATPase
Calcium
Journal Article Review

Word Cloud

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