Abstract
Accounting for almost one-third of the global mortality, cardiovascular diseases (CVDs) represent a major global health issue. Emerging data suggest that most of the well-established mechanistic explanations regarding the cardiovascular pathophysiology are flawed, and cannot fully explain the progression and long-term effects of these diseases. On the other hand, dysregulation of the sympathetic nervous system (SNS) has emerged as an important player in the pathophysiology of CVDs. Even though upregulated SNS activity is an essential compensatory response to various stress conditions, in the long term, it becomes a major contributor to both cardiac dysfunction and vascular damage. Despite the fact that the importance of SNS hyperactivity in the setting of CVDs has been well-appreciated, its exact quantification and clinical application in either diagnostics or therapy of CVDs is still out of reach. Nevertheless, in recent years a number of novel laboratory biomarkers implicated in the pathophysiology of SNS activation have been explored. Specifically, in this review, we aimed to discuss the role of catestatin, a potent physiological inhibitor of catecholamine spillover that offers cardioprotective effects. Limited data indicate that catestatin could also be a reliable indirect marker of SNS activity and it is likely that high CST levels reflect advanced CV disease burden. Consequently, large-scale studies are required to validate these observations in the upcoming future.
Highlights
Accounting for almost a third of the global mortality, cardiovascular diseases (CVDs), an umbrella term for several linked pathologies of the CV system, still represent a major global health issue [1]
Initially identified as a physiological inhibitor of catecholamine secretion, catestatin has recently emerged as a potent pleiotropic peptide that leads to a reduction in arterial blood pressure, and positively regulates baroreflex sensitivity and heart rate variability, providing cardioprotection
The data suggest that various single nucleotide polymorphisms (SNPs) present in the catestatin-expressing region of the CHGA gene in different human populations lead to different variants of catestatin [25]
Summary
Accounting for almost a third of the global mortality, cardiovascular diseases (CVDs), an umbrella term for several linked pathologies of the CV system, still represent a major global health issue [1]. The emerging data suggest that most of the wellestablished mechanistic explanations regarding the CV pathophysiology are flawed, and cannot fully explain the progression and long-term effects of these diseases [2]. Biomedicines 2021, 9, 1757 as important players in the pathophysiology of CVDs, notably in regard to heart failure (HF) [3]. SNS activation is one of the fundamental responses of the human body to stress, which acts by inducing and/or modifying a wide spectrum of potent hemodynamic effects, including positive inotropic, lusitropic, chronotropic, and dromotropic effects on the heart, as well as centralization of the blood flow via vasoconstriction [4]. Initially identified as a physiological inhibitor of catecholamine secretion, catestatin has recently emerged as a potent pleiotropic peptide that leads to a reduction in arterial blood pressure, and positively regulates baroreflex sensitivity and heart rate variability, providing cardioprotection
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
