Cargando…

The Involvement of Calcium Channels in the Endoplasmic Reticulum Membrane in Nonalcoholic Fatty Liver Disease Pathogenesis

Nonalcoholic fatty liver disease (NAFLD) is a prevalent and complex condition that affects millions of people globally. It occurs when fat, primarily triglycerides, accumulates in liver cells, leading to inflammation and damage. Calcium, an essential mineral, is involved in various physiological pro...

Descripción completa

Detalles Bibliográficos
Autores principales: Albalawi, Sarah S, Aljabri, Ahmed, Alshibani, Mohannad, Al-Gayyar, Mohammed M
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10663096/
https://www.ncbi.nlm.nih.gov/pubmed/38024063
http://dx.doi.org/10.7759/cureus.49150
_version_ 1785148623151955968
author Albalawi, Sarah S
Aljabri, Ahmed
Alshibani, Mohannad
Al-Gayyar, Mohammed M
author_facet Albalawi, Sarah S
Aljabri, Ahmed
Alshibani, Mohannad
Al-Gayyar, Mohammed M
author_sort Albalawi, Sarah S
collection PubMed
description Nonalcoholic fatty liver disease (NAFLD) is a prevalent and complex condition that affects millions of people globally. It occurs when fat, primarily triglycerides, accumulates in liver cells, leading to inflammation and damage. Calcium, an essential mineral, is involved in various physiological processes, including the regeneration process following liver injury. The endoplasmic reticulum (ER), a complex organelle involved in protein synthesis and lipid metabolism, regulates intracellular calcium levels. Dysregulation of this process can lead to calcium overload, oxidative stress, and cellular damage, all of which are hallmarks of NAFLD. Inositol 1,4,5-trisphosphate receptor (IP3R), a type of calcium ion channel, is found throughout the body, including the liver. IP3R is classified into three subtypes: IP3R1, IP3R2, and IP3R3, and it plays a critical role in regulating intracellular calcium levels. However, excessive calcium accumulation in the mitochondria due to an overload of calcium ions or increased IP3R activity can lead to NAFLD. Therefore, targeting calcium channels in the ER membrane may represent a promising therapeutic strategy for preventing and treating this increasingly prevalent metabolic disorder. It may help prevent mitochondrial calcium accumulation and reduce the risk of hepatic damage. This review article aimed to review the relationship between IP3R modulation and the pathogenicity of NAFLD, providing valuable insights to help researchers develop more effective treatments for the condition.
format Online
Article
Text
id pubmed-10663096
institution National Center for Biotechnology Information
language English
publishDate 2023
publisher Cureus
record_format MEDLINE/PubMed
spelling pubmed-106630962023-11-20 The Involvement of Calcium Channels in the Endoplasmic Reticulum Membrane in Nonalcoholic Fatty Liver Disease Pathogenesis Albalawi, Sarah S Aljabri, Ahmed Alshibani, Mohannad Al-Gayyar, Mohammed M Cureus Gastroenterology Nonalcoholic fatty liver disease (NAFLD) is a prevalent and complex condition that affects millions of people globally. It occurs when fat, primarily triglycerides, accumulates in liver cells, leading to inflammation and damage. Calcium, an essential mineral, is involved in various physiological processes, including the regeneration process following liver injury. The endoplasmic reticulum (ER), a complex organelle involved in protein synthesis and lipid metabolism, regulates intracellular calcium levels. Dysregulation of this process can lead to calcium overload, oxidative stress, and cellular damage, all of which are hallmarks of NAFLD. Inositol 1,4,5-trisphosphate receptor (IP3R), a type of calcium ion channel, is found throughout the body, including the liver. IP3R is classified into three subtypes: IP3R1, IP3R2, and IP3R3, and it plays a critical role in regulating intracellular calcium levels. However, excessive calcium accumulation in the mitochondria due to an overload of calcium ions or increased IP3R activity can lead to NAFLD. Therefore, targeting calcium channels in the ER membrane may represent a promising therapeutic strategy for preventing and treating this increasingly prevalent metabolic disorder. It may help prevent mitochondrial calcium accumulation and reduce the risk of hepatic damage. This review article aimed to review the relationship between IP3R modulation and the pathogenicity of NAFLD, providing valuable insights to help researchers develop more effective treatments for the condition. Cureus 2023-11-20 /pmc/articles/PMC10663096/ /pubmed/38024063 http://dx.doi.org/10.7759/cureus.49150 Text en Copyright © 2023, Albalawi et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Gastroenterology
Albalawi, Sarah S
Aljabri, Ahmed
Alshibani, Mohannad
Al-Gayyar, Mohammed M
The Involvement of Calcium Channels in the Endoplasmic Reticulum Membrane in Nonalcoholic Fatty Liver Disease Pathogenesis
title The Involvement of Calcium Channels in the Endoplasmic Reticulum Membrane in Nonalcoholic Fatty Liver Disease Pathogenesis
title_full The Involvement of Calcium Channels in the Endoplasmic Reticulum Membrane in Nonalcoholic Fatty Liver Disease Pathogenesis
title_fullStr The Involvement of Calcium Channels in the Endoplasmic Reticulum Membrane in Nonalcoholic Fatty Liver Disease Pathogenesis
title_full_unstemmed The Involvement of Calcium Channels in the Endoplasmic Reticulum Membrane in Nonalcoholic Fatty Liver Disease Pathogenesis
title_short The Involvement of Calcium Channels in the Endoplasmic Reticulum Membrane in Nonalcoholic Fatty Liver Disease Pathogenesis
title_sort involvement of calcium channels in the endoplasmic reticulum membrane in nonalcoholic fatty liver disease pathogenesis
topic Gastroenterology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10663096/
https://www.ncbi.nlm.nih.gov/pubmed/38024063
http://dx.doi.org/10.7759/cureus.49150
work_keys_str_mv AT albalawisarahs theinvolvementofcalciumchannelsintheendoplasmicreticulummembraneinnonalcoholicfattyliverdiseasepathogenesis
AT aljabriahmed theinvolvementofcalciumchannelsintheendoplasmicreticulummembraneinnonalcoholicfattyliverdiseasepathogenesis
AT alshibanimohannad theinvolvementofcalciumchannelsintheendoplasmicreticulummembraneinnonalcoholicfattyliverdiseasepathogenesis
AT algayyarmohammedm theinvolvementofcalciumchannelsintheendoplasmicreticulummembraneinnonalcoholicfattyliverdiseasepathogenesis
AT albalawisarahs involvementofcalciumchannelsintheendoplasmicreticulummembraneinnonalcoholicfattyliverdiseasepathogenesis
AT aljabriahmed involvementofcalciumchannelsintheendoplasmicreticulummembraneinnonalcoholicfattyliverdiseasepathogenesis
AT alshibanimohannad involvementofcalciumchannelsintheendoplasmicreticulummembraneinnonalcoholicfattyliverdiseasepathogenesis
AT algayyarmohammedm involvementofcalciumchannelsintheendoplasmicreticulummembraneinnonalcoholicfattyliverdiseasepathogenesis