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Heart Fail Rev. 2018 Mar;23(2):261-272. doi: 10.1007/s10741-018-9676-1.

Protein tyrosine phosphatases in cardiac physiology and pathophysiology.

Author information

1
Cardiovascular Research Program, King Faisal Specialist Hospital and Research Centre, PO Box 3354, Riyadh, 11211, Saudi Arabia.
2
College of Medicine and Health Sciences, Al-Faisal University, Riyadh, 11211, Saudi Arabia.
3
Cardiovascular Research Program, King Faisal Specialist Hospital and Research Centre, PO Box 3354, Riyadh, 11211, Saudi Arabia. coralie.poizat@gmail.com.
4
Biology Department, San Diego State University, San Diego, CA, 92182, USA. coralie.poizat@gmail.com.

Abstract

More than any other organ, the heart is particularly sensitive to gene expression deregulation, often leading in the long run to impaired contractile performances and excessive fibrosis deposition progressing to heart failure. Recent investigations provide evidences that the protein phosphatases (PPs), as their counterpart protein kinases, are important regulators of cardiac physiology and development. Two main groups, the protein serine/threonine phosphatases and the protein tyrosine phosphatases (PTPs), constitute the PPs family. Here, we provide an overview of the role of PTP subfamily in the development of the heart and in cardiac pathophysiology. Based on recent in silico studies, we highlight the importance of PTPs as therapeutic targets for the development of new drugs to restore PTPs signaling in the early and late events of heart failure.

KEYWORDS:

Cardiac hypertrophy; Heart failure; PTP; Protein tyrosine phosphatase; Small-molecule inhibitor

PMID:
29396779
PMCID:
PMC5861171
DOI:
10.1007/s10741-018-9676-1
[Indexed for MEDLINE]
Free PMC Article

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