Macromolecular Degradation Systems and Cardiovascular Aging
Author(s) -
Hiroyuki Nakayama,
Kazuhiko Nishida,
Kinya Otsu
Publication year - 2016
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/circresaha.115.307495
Subject(s) - senescence , inflammation , proinflammatory cytokine , mechanism (biology) , reactive oxygen species , intracellular , angiotensin ii , medicine , fibrosis , biology , microbiology and biotechnology , blood pressure , philosophy , epistemology
Aging-related cardiovascular diseases are a rapidly increasing problem worldwide. Cardiac aging demonstrates progressive decline of diastolic dysfunction of ventricle and increase in ventricular and arterial stiffness accompanied by increased fibrosis stimulated by angiotensin II and proinflammatory cytokines. Reactive oxygen species and multiple signaling pathways on cellular senescence play major roles in the process. Aging is also associated with an alteration in steady state of macromolecular dynamics including a dysfunction of protein synthesis and degradation. Currently, impaired macromolecular degradation is considered to be closely related to enhanced inflammation and be involved in the process and mechanism of cardiac aging. Herein, we review the role and mechanisms of the degradation system of intracellular macromolecules in the process and pathophysiology of cardiovascular aging.
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