The Role of CD38 in the Pathogenesis of Cardiorenal Metabolic Disease and Aging, an Approach from Basic Research

Author:

Kitada Munehiro12,Araki Shin-ichi2,Koya Daisuke34

Affiliation:

1. Department of Internal Medicine, Hamada Neurosurgery and Internal Medicine Clinic, Wakayama 641-8509, Japan

2. Department of Nephrology, Wakayama Medical University, Wakayama 641-8509, Japan

3. Omi Medical Center, Kusatsu, Shiga 525-8585, Japan

4. Division of Anticipatory Molecular Food Science and Technology, Medical Research Institute, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan

Abstract

Aging is a major risk factor for the leading causes of mortality, and the incidence of age-related diseases including cardiovascular disease, kidney disease and metabolic disease increases with age. NAD+ is a classic coenzyme that exists in all species, and that plays a crucial role in oxidation–reduction reactions. It is also involved in the regulation of many cellular functions including inflammation, oxidative stress and differentiation. NAD+ declines with aging in various organs, and the reduction in NAD+ is possibly involved in the development of age-related cellular dysfunction in cardiorenal metabolic organs through the accumulation of inflammation and oxidative stress. Levels of NAD+ are regulated by the balance between its synthesis and degradation. CD38 is the main NAD+-degrading enzyme, and CD38 is activated in response to inflammation with aging, which is associated with the reduction in NAD+ levels. In this review, focusing on CD38, we discuss the role of CD38 in aging and the pathogenesis of age-related diseases, including cardiorenal metabolic disease.

Funder

KAKENHI, Grant-in-Aid for Challenging Exploratory Research

KAKENHI, Grant-in-Aid for Scientific Research

Publisher

MDPI AG

Subject

General Medicine

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