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TMAO accelerates cellular aging by disrupting endoplasmic reticulum integrity and mitochondrial unfolded protein response.
Cell Mol Life Sci
January 2025
Department of Medicine, Wilf Family Cardiovascular Research Institute, Institute for Neuroimmunology and Inflammation (INI), Einstein Institute for Aging Research, New York, NY, USA.
Trimethylamine-N-oxide accelerates osteoporosis by PERK activation of ATF5 unfolding.
Cell Mol Life Sci
December 2024
Center for Mitochondrial Research and Medicine, College of Medicine Chang Gung University, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
Imbalances in gut microbiota and their metabolites have been implicated in osteoporotic disorders. Trimethylamine-n-oxide (TMAO), a metabolite of L-carnitine produced by gut microorganisms and flavin-containing monooxygenase-3, is known to accelerate tissue metabolism and remodeling; however, its role in bone loss remained unexplored. This study investigates the relationship between gut microbiota dysbiosis, TMAO production, and osteoporosis development.
View Article and Find Full Text PDFTrimethylamine N-oxide in cardiovascular disease: Pathophysiology and the potential role of statins.
Life Sci
January 2025
Department of Internal Medicine, Metropolitan Hospital Center, New York, NY, USA. Electronic address:
Cardiovascular diseases are one of the leading causes of mortality and morbidity worldwide, with the total number of cases increasing to 523 million in 2019. Despite the advent of new drugs, cardiovascular mortality has increased at an alarming rate of 53.7 % from 12.
View Article and Find Full Text PDFTrimethylamine N-oxide promotes PERK-mediated endothelial-mesenchymal transition and apoptosis thereby aggravates atherosclerosis.
Int Immunopharmacol
December 2024
Department of Cardiovascular, Ningbo Medical Center Lihuili Hospital, Ningbo University, Ningbo, China; Ningbo Institute of Innovation for Combined Medicine and Engineering, Ningbo, China. Electronic address:
The endothelial-mesenchymal transition (EndMT) is involved in the development of atherosclerosis (AS) and is a key process in vascular endothelial injury. Oxidative stress, inflammation, and apoptosis are common causes of EndMT, and EndMT progression can further accelerate the development of AS. The metabolite trimethylamine N-oxide (TMAO) is produced by the gut microbiome and is implicated in the development of several diseases, including diabetes and chronic kidney disease.
View Article and Find Full Text PDFSmall organic osmolytes accelerate actin filament assembly and stiffen filaments.
Cytoskeleton (Hoboken)
September 2024
NanoScience Technology Center, University of Central Florida, Orlando, Florida, USA.
Actin filament assembly and mechanics are crucial for maintenance of cell structure, motility, and division. Actin filament assembly occurs in a crowded intracellular environment consisting of various types of molecules, including small organic molecules known as osmolytes. Ample evidence highlights the protective functions of osmolytes such as trimethylamine-N-oxide (TMAO), including their effects on protein stability and their ability to counteract cellular osmotic stress.
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