Activation of the sirtuin silent information regulator 1 pathway inhibits pathological myocardial remodeling

Abstract

Myocardial remodeling refers to structural and functional disorders of the heart caused by molecular biological changes in the cardiac myocytes in response to neurological and humoral factors. A variety of heart diseases, such as hypertension, coronary artery disease, arrhythmia, and valvular heart disease, can cause myocardial remodeling and eventually lead to heart failure. Therefore, counteracting myocardial remodeling is essential for the prevention and treatment of heart failure. Sirt1 is a nicotinamide adenine dinucleotide+-dependent deacetylase that plays a wide range of roles in transcriptional regulation, energy metabolism regulation, cell survival, DNA repair, inflammation, and circadian regulation. It positively or negatively regulates myocardial remodeling by participating in oxidative stress, apoptosis, autophagy, inflammation, and other processes. Taking into account the close relationship between myocardial remodeling and heart failure and the involvement of SIRT1 in the development of the former, the role of SIRT1 in the prevention of heart failure via inhibition of myocardial remodeling has received considerable attention. Recently, multiple studies have been conducted to provide a better understanding of how SIRT1 regulates these phenomena. This review presents the progress of research involving SIRT1 pathway involvement in the pathophysiological mechanisms of myocardial remodeling and heart failure.

Investigating the potential neuroprotective benefits of taurine and Dihydrotestosterone and Hydroxyprogesterone levels in SH-SY5Y cells

“…Progesterone, primarily produced in the ovaries, has demonstrated its neuroprotective capabilities in various disease models, including AD, stroke, and traumatic brain injury ( Stein et al, 2008 ; Singh and Su, 2013 ; Canfrán-Duque et al, 2017 ). Taurine has been shown to increase Sirtuin 1 gene expression in various cells such as the liver and heart ( Feng et al, 2018 ; Wang et al, 2023 ). In our experiments, LPS concentration may control DHT and DHP levels by affecting Sirtuin 1 gene expression.…”

The Current State of Research on Sirtuin-Mediated Autophagy in Cardiovascular Diseases

“…The knockout of FGF21, the inhibition of autophagy by 3-methyladenine (3MA), or the inhibition of SIRT1 by sirtinol abolishes the therapeutic effects of FF. These findings suggest that FF prevents type 1 diabetes-induced cardiac pathology and functional abnormalities by increasing FGF21 expression and upregulating SIRT1-mediated autophagy [ 138 ] ( Table 1 , Figure 4 ).…”

SIRT1 activation promotes energy homeostasis and reprograms liver cancer metabolism

“…SIRT1 is a well-studied member of the sirtuin family and is known as a stress-responsive protein deacetylase [4]. Numerous studies have described the potential role of SIRT1 functions in DNA repair, oxidative stress response, metabolism, circadian control, and mitochondrial biogenesis [5][6][7]. Today, SIRT1 is targeted in many age-related human pathologies, such as cardiovascular disease, diabetes and other metabolic syndromes, chronic inflammation, neurodegenerative disorders, and cancer [8].…”