SMP30 and Aging-Related Cardiac Remodeling and Heart Failure

Abstract

The expression of senescence marker protein 30 (SMP30) decreases androgen independently with aging. SMP30 is expressed mainly in liver and renal proximal tubular epithelium in higher animal species. The human SMP30 gene is present on the X chromosome, and its molecular weight is almost 34 kDa. SMP30 is multifunctional. SMP30 is the same as regucalcin which plays a role in the regulation of Ca2+ homeostasis and is the same as gluconolactonase, which is involved in ascorbic acid biosynthesis. SMP30 knockout mice are used to elucidate various physiological functions of SMP30. These mice showed shorter lifespan than the control wild-type mice and definitely malnutrition and emaciation. Antioxidative effects of SMP30 in various organs including brain and lung were reported with the use of these mice. SMP30 protein expression is enhanced by a calorie restriction diet, and downregulation of SMP30 was accompanied by increased generation of reactive oxygen species. Therefore, the association of SMP30 and oxidative stress is a key component for the elucidation of the association of SMP30 and age-related stress disease. We demonstrated antiapoptotic effects in addition to the antioxidative effects of SMP30 in aging-related cardiac remodeling, which are associated with the renin–angiotensin–aldosterone system activation. This examination demonstrated that SMP30 could have a cardioprotective effect similar to the protective effect seen in other organs, and SMP30 might be one of the therapeutic key components for cardiac remodeling accelerated by oxidative stress and aging.