Maiese K. Cardiovascular and nonalcoholic fatty liver disease: Sharing common ground through SIRT1 pathways. World J Cardiol 2024; 16(11): 632-643 [DOI: 10.4330/wjc.v16.i11.632]
Corresponding Author of This Article
Kenneth Maiese, MD, National Heart, Lung, and Blood Institute, National Institutes of Health, Cellular and Molecular Signaling, Bethesda, MD 20810, United States. wntin75@yahoo.com
Research Domain of This Article
Cell Biology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Cardiol. Nov 26, 2024; 16(11): 632-643 Published online Nov 26, 2024. doi: 10.4330/wjc.v16.i11.632
Cardiovascular and nonalcoholic fatty liver disease: Sharing common ground through SIRT1 pathways
Kenneth Maiese
Kenneth Maiese, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20810, United States
Author contributions: Maiese K conceived, designed, and wrote this article.
Supported by American Diabetes Association; American Heart Association; NIH NIEHS; NIH NIA; NIH NINDS; NS053956; and NIH ARRA.
Conflict-of-interest statement: The author reports no conflicts of interest for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Kenneth Maiese, MD, National Heart, Lung, and Blood Institute, National Institutes of Health, Cellular and Molecular Signaling, Bethesda, MD 20810, United States. wntin75@yahoo.com
Received: July 13, 2024 Revised: August 27, 2024 Accepted: October 10, 2024 Published online: November 26, 2024 Processing time: 109 Days and 17.2 Hours
Abstract
As a non-communicable disease, cardiovascular disorders have become the leading cause of death for men and women. Of additional concern is that cardiovascular disease is linked to chronic comorbidity disorders that include nonalcoholic fatty liver disease (NAFLD). NAFLD, also termed metabolic-dysfunction-associated steatotic liver disease, is the greatest cause of liver disease throughout the world, increasing in prevalence concurrently with diabetes mellitus (DM), and can progress to nonalcoholic steatohepatitis that leads to cirrhosis and liver fibrosis. Individuals with metabolic disorders, such as DM, are more than two times likely to experience cardiac disease, stroke, and liver disease that includes NAFLD when compared individuals without metabolic disorders. Interestingly, cardiovascular disorders and NAFLD share a common underlying cellular mechanism for disease pathology, namely the silent mating type information regulation 2 homolog 1 (SIRT1; Saccharomyces cerevisiae). SIRT1, a histone deacetylase, is linked to metabolic pathways through nicotinamide adenine dinucleotide and can offer cellular protection though multiple avenues, including trophic factors such as erythropoietin, stem cells, and AMP-activated protein kinase. Translating SIRT1 pathways into clinical care for cardiovascular and hepatic disease can offer significant hope for patients, but further insights into the complexity of SIRT1 pathways are necessary for effective treatment regimens.
Core Tip: Cardiovascular disease is the principal cause of non-communicable diseases with individuals succumbing to heart disease every thirty-three seconds and has a significant comorbidity with nonalcoholic fatty liver disease (NAFLD). These two disorders impact millions of individuals across the globe, yield significant disability and death to individuals, and have a common underlying cellular pathway with silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) that may offer innovative prospects for the treatment of both cardiovascular disorders and NAFLD.
