ER calcium release promotes mitochondrial dysfunction and hepatic cell lipotoxicity in response to palmitate overload-Reference-Cited by-同舟云学术

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ER calcium release promotes mitochondrial dysfunction and hepatic cell lipotoxicity in response to palmitate overload

Published:2014-08 Issue:5 Volume:3 Page:544-553
ISSN:2212-8778
Container-title:Molecular Metabolism
language:en
Short-container-title:Molecular Metabolism

Author:

Egnatchik Robert A.,Leamy Alexandra K.,Jacobson David A.,Shiota Masakazu,Young Jamey D.

Funder

National Science Foundation

Vanderbilt Diabetes Research and Training Center

Publisher

Elsevier BV

Subject

Cell Biology,Molecular Biology

Reference38 articles.

1. Aberrant lipid metabolism disrupts calcium homeostasis causing liver endoplasmic reticulum stress in obesity;Fu;Nature,2011

2. Excessive hepatic mitochondrial TCA cycle and gluconeogenesis in humans with nonalcoholic fatty liver disease;Sunny;Cell Metabolism,2011

3. Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes;Ozcan;Science,2004

4. Elevated TCA cycle function in the pathology of diet-induced hepatic insulin resistance and fatty liver;Satapati;Journal of Lipid Research,2012

5. Hepatocyte apoptosis and Fas expression are prominent features of human nonalcoholic steatohepatitis;Feldstein;Gastroenterology,2003

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1. Targeting BRD4 mitigates hepatocellular lipotoxicity by suppressing the NLRP3 inflammasome activation and GSDMD-mediated hepatocyte pyroptosis;Cellular and Molecular Life Sciences;2024-07-09

2. Non-esterified fatty acid palmitate facilitates oxidative endoplasmic reticulum stress and apoptosis of β-cells by upregulating ERO-1α expression;Redox Biology;2024-07

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