Catestatin: A Master Regulator of Cardiovascular Functions

被引:50
作者
Mahata, Sushil K. [1 ,2 ]
Kiranmayi, Malapaka [3 ]
Mahapatra, Nitish R. [3 ]
机构
[1] VA San Diego Healthcare Syst, Metab Physiol & Ultrastruct Biol Lab, 3350 La Jolla Village Dr, San Diego, CA 92161 USA
[2] Univ Calif San Diego, Metab Physiol & Ultrastruct Biol Lab, 9500 Gilman Dr, La Jolla, CA 92093 USA
[3] Indian Inst Technol, Bhupat & Jyoti Mehta Sch Biosci, Dept Biotechnol, Madras 600036, Tamil Nadu, India
关键词
Chromogranin A; adrenergic beta-2 receptor; cardiomyopathy; cardioprotection; heart failure; hypertension; immune cells; nicotinic-cholinergic receptor; RELEASE-INHIBITORY PEPTIDE; CHROMOGRANIN-A FRAGMENT; TUMOR-NECROSIS-FACTOR; ISCHEMIA-REPERFUSION INJURY; PROTEOLYTIC CLEAVAGE SITES; FRANK-STARLING RESPONSE; NITRIC-OXIDE SYNTHASE; T-CELL-ACTIVATION; CATECHOLAMINE-RELEASE; HEART-FAILURE;
D O I
10.2174/0929867324666170425100416
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: Cardiovascular disease (CVD), the most common cause of death globally, accounts for similar to 30% of all deaths worldwide. Hypertension is a common contributor to morbidity and mortality from CVD. Methods and Results: The plasma concentration of chromogranin A (CgA) is elevated in patients with CVD as well as patients with established human essential hypertension and heart failure (HF). In contrast, the plasma level of the CgA-derived peptide catestatin (CST) is diminished in human essential hypertension. Low conversion of CgA-to-CST has been associated with increased mortality in patients hospitalized with acute HF. Consistent with human findings, the lack of CST in CgA knockout (Chga-KO) mice eventuates in the development of hypertension and supplementation of CST to Chga-KO mice restores blood pressure, implicating CST as a key player in regulating hypertension. In the peripheral system, CST decreases blood pressure by stimulating histamine release, inhibiting catecholamine secretion, or causing vasodilation. Centrally, CST improves baroreflex sensitivity (BRS) and heart rate variability (HRV) by exciting GABAergic neurons in the caudal ventrolateral medulla (CVLM) and pyramidal neurons of the central amygdala; CST also decreases BRS by exciting glutamatergic rostral ventrolateral medulla (RVLM) neurons. In addition, CST provides cardioprotection by inhibiting inotropy and lusitropy; activating mitochondrial K-ATP channels, and stimulating reperfusion injury salvage kinase (RISK) and survivor activating factor enhancement (SAFE) pathways and consequent inhibition of mitochondrial permeability transition pore (mPTP). CST modulates cardiomyocyte Ca2+ levels by direct inhibition of Ca2+/calmodulin-dependent protein kinase Ho (CaMKII delta) activity and consequent reduction in phosphorylation of phospholamban and ryanodine receptor 2, thereby providing support for a direct functional role of CST in the failing myocardium. Conclusion: These multitude of effects establish CST as a master regulator of cardiovascular functions.
引用
收藏
页码:1352 / 1374
页数:23
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