Version 1
: Received: 27 August 2023 / Approved: 28 August 2023 / Online: 29 August 2023 (03:39:04 CEST)
How to cite:
Kumar, R. Cholesterol Homeostasis, Mechanisms of Molecular Pathways, and Cardiac Health. Preprints2023, 2023081889. https://doi.org/10.20944/preprints202308.1889.v1
Kumar, R. Cholesterol Homeostasis, Mechanisms of Molecular Pathways, and Cardiac Health. Preprints 2023, 2023081889. https://doi.org/10.20944/preprints202308.1889.v1
Kumar, R. Cholesterol Homeostasis, Mechanisms of Molecular Pathways, and Cardiac Health. Preprints2023, 2023081889. https://doi.org/10.20944/preprints202308.1889.v1
APA Style
Kumar, R. (2023). Cholesterol Homeostasis, Mechanisms of Molecular Pathways, and Cardiac Health. Preprints. https://doi.org/10.20944/preprints202308.1889.v1
Chicago/Turabian Style
Kumar, R. 2023 "Cholesterol Homeostasis, Mechanisms of Molecular Pathways, and Cardiac Health" Preprints. https://doi.org/10.20944/preprints202308.1889.v1
Abstract
The metabolism of lipoproteins, which regulates the transit of the lipid to and from tissues, is crucial to maintaining cholesterol homeostasis. Cardiac remodeling is referred to as a set of molecular, cellular, and interstitial changes that, following injury, affect the size, shape, function, mass, and geometry of the heart. Acetyl coenzyme A (acetyl CoA), which can be made from glucose, amino acids, or fatty acids, is the precursor for the synthesis of cholesterol. In this article, authors explain concepts behind cardiac remodeling, its clinical ramifications, and the pathophysiological roles played by numerous various components, such as cell death, neurohormonal activation, oxidative stress, contractile proteins, energy metabolism, collagen, calcium transport, inflammation, and geometry. The levels of cholesterol are traditionally regulated by two biological mechanisms at the transcriptional stage. First, the SREBP transcription factor family regulates the transcription of crucial rate-limiting cholesterogenic and lipogenic proteins, which in turn limits cholesterol production. Immune cells become activated, differentiated, and divided, during an immune response with the objective of eradicating the danger signal. In addition to creating ATP, which is used as energy, this process relies on metabolic reprogramming of both catabolic and anabolic pathways to create metabolites that play a crucial role in regulating the response. Because of changes in signal transduction, malfunction of the sarcoplasmic reticulum and sarcolemma, impairment of calcium handling, increases in cardiac fibrosis, and progressive loss of cardiomyocytes, oxidative stress appears to be the primary mechanism that causes the transition from cardiac hypertrophy to heart failure. De novo cholesterol production, intestinal cholesterol absorption, and biliary cholesterol output are consequently crucial processes in cholesterol homeostasis. In the article's final section, the pharmacological management of cardiac remodeling is explored. The route of treatment is explained into different steps: including, promising, and potential strategies. This chapter offers a brief overview of the history of the study of cholesterol absorption as well as the different potential therapeutic targets.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
