Editorial...
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Hindawi Publishing Corporation Biochemistry Research International Volume 2012, Article ID 257528, 2 pages doi:10.1155/2012/257528 Editorial Endoplasmic Reticulum Stress and Lipid Metabolism Huiping Zhou, 1, 2 Kezhong Zhang, 3, 4 Sabina Janciauskiene, 5 and Xiaokun Li 6 1 Department of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USA 2 Hunter Holmes McGuire VA Medical Center, Richmond, VA 23298, USA 3 Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA 4 Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI 48201, USA 5 Department of Respiratory Medicine, Hannover Medical School, Feodor Lynen Street 23, 30625 Hannover, Germany 6 College of Pharmacy, Wenzhou Medical College, Wenzhou, Zhejiang 325035, China Correspondence should be addressed to Huiping Zhou, [email protected] Received 12 April 2012; Accepted 12 April 2012 Copyright © 2012 Huiping Zhou et al. 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. Endoplasmic reticulum (ER) is an elaborate cellular organelle essential for protein folding, calcium homeosta- sis, and lipid biosynthesis. Disruption of ER homeostasis imposes stress on the ER and subsequently leads to accumu- lation of unfolded or misfolded proteins in the ER lumen—a condition termed ER stress. In response to ER stress, a group of intracellular signaling pathways originated from the ER, collectively termed ER stress response, are activated to alter transcriptional and translational programs in the stressed cells. ER stress response has been linked to various human diseases associated with dyslipidemia, such as inflammatory diseases, obesity, diabetes, alcoholic and nonalcoholic liver diseases, and cardiovascular diseases. Understanding the impact of ER stress signaling pathways on lipid metabolism will provide important information for the prevention and treatment of these common human diseases in the modern world. The paper by C. Ji provided an updated overview of the potential mechanisms involved in alcohol-induced ER stress and organ injuries. The alcoholic injuries and roles of ER stress in major organs including liver, pancreas, brain, and heart were discussed. In addition, several important mechanisms underlying alcohol-induced ER stress were described in detail. The paper by S. Basseri and R. C. Austin provided an overview of recent findings related to ER stress and hepatic lipid metabolism. Liver is the central organ involved in lipid metabolism. Disruption of hepatic lipid metabolism has been linked to various metabolic diseases. Regulation of hepatic lipid metabolism and ER-stress signaling pathways was described. Furthermore, the therapeutic potential of targeting ER stress signaling pathways in dyslipidemia and obesity was discussed. The paper by E. B. Thorp discussed the Unfolded- Protein-Response-(UPR)-induced apoptosis in ischemic car- diovascular disease. Ischemia is the major cause of heart failure which is secondary to dyslipidemia, atherosclerosis, and myocardial infarction. The ER stress signaling pathways in cardiomyocyte and role of ER stress in ischemia-induced apoptosis were discussed. The paper by J. W. Brewer and S. Jackowski focused on the physiological UPR in the regulation of lipid synthesis and membrane biogenesis during the differentiation of B lymphocytes into antibody-secreting plasma cells. This paper described the current understanding of the relation- ship between the UPR, lipid biosynthesis, and organelle biogenesis in activated B cells. In particular, the authors provided up-to-date information regarding the roles and mechanisms of the UPR signaling pathways in regulating phosphatidylcholine synthesis and ER biosynthesis. The paper by X. Zhang and K. Zhang discussed the links between ER stress, lipid droplet formation, and type II diabetes. The excessive deposition of lipid droplets in adipocytes, hepatocytes, and macrophages has been recog- nized as a feature of many metabolic diseases, including type II diabetes. Increasing evidence suggests that ER stress response regulates the lipid droplet formation that is associated with the pathogenesis of type II diabetes. This
Transcript of Editorial...
Hindawi Publishing CorporationBiochemistry Research InternationalVolume 2012, Article ID 257528, 2 pagesdoi:10.1155/2012/257528
Editorial
Endoplasmic Reticulum Stress and Lipid Metabolism
Huiping Zhou,1, 2 Kezhong Zhang,3, 4 Sabina Janciauskiene,5 and Xiaokun Li6
1 Department of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University,Richmond, VA 23298, USA
2 Hunter Holmes McGuire VA Medical Center, Richmond, VA 23298, USA3 Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA4 Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI 48201, USA5 Department of Respiratory Medicine, Hannover Medical School, Feodor Lynen Street 23, 30625 Hannover, Germany6 College of Pharmacy, Wenzhou Medical College, Wenzhou, Zhejiang 325035, China
Correspondence should be addressed to Huiping Zhou, [email protected]
Received 12 April 2012; Accepted 12 April 2012
Copyright © 2012 Huiping Zhou et al. 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.
Endoplasmic reticulum (ER) is an elaborate cellularorganelle essential for protein folding, calcium homeosta-sis, and lipid biosynthesis. Disruption of ER homeostasisimposes stress on the ER and subsequently leads to accumu-lation of unfolded or misfolded proteins in the ER lumen—acondition termed ER stress. In response to ER stress, a groupof intracellular signaling pathways originated from the ER,collectively termed ER stress response, are activated to altertranscriptional and translational programs in the stressedcells. ER stress response has been linked to various humandiseases associated with dyslipidemia, such as inflammatorydiseases, obesity, diabetes, alcoholic and nonalcoholic liverdiseases, and cardiovascular diseases. Understanding theimpact of ER stress signaling pathways on lipid metabolismwill provide important information for the prevention andtreatment of these common human diseases in the modernworld.
The paper by C. Ji provided an updated overview of thepotential mechanisms involved in alcohol-induced ER stressand organ injuries. The alcoholic injuries and roles ofER stress in major organs including liver, pancreas, brain,and heart were discussed. In addition, several importantmechanisms underlying alcohol-induced ER stress weredescribed in detail.
The paper by S. Basseri and R. C. Austin provided anoverview of recent findings related to ER stress and hepaticlipid metabolism. Liver is the central organ involved inlipid metabolism. Disruption of hepatic lipid metabolismhas been linked to various metabolic diseases. Regulation of
hepatic lipid metabolism and ER-stress signaling pathwayswas described. Furthermore, the therapeutic potential oftargeting ER stress signaling pathways in dyslipidemia andobesity was discussed.
The paper by E. B. Thorp discussed the Unfolded-Protein-Response-(UPR)-induced apoptosis in ischemic car-diovascular disease. Ischemia is the major cause of heartfailure which is secondary to dyslipidemia, atherosclerosis,and myocardial infarction. The ER stress signaling pathwaysin cardiomyocyte and role of ER stress in ischemia-inducedapoptosis were discussed.
The paper by J. W. Brewer and S. Jackowski focused onthe physiological UPR in the regulation of lipid synthesisand membrane biogenesis during the differentiation ofB lymphocytes into antibody-secreting plasma cells. Thispaper described the current understanding of the relation-ship between the UPR, lipid biosynthesis, and organellebiogenesis in activated B cells. In particular, the authorsprovided up-to-date information regarding the roles andmechanisms of the UPR signaling pathways in regulatingphosphatidylcholine synthesis and ER biosynthesis.
The paper by X. Zhang and K. Zhang discussed thelinks between ER stress, lipid droplet formation, and typeII diabetes. The excessive deposition of lipid droplets inadipocytes, hepatocytes, and macrophages has been recog-nized as a feature of many metabolic diseases, includingtype II diabetes. Increasing evidence suggests that ERstress response regulates the lipid droplet formation that isassociated with the pathogenesis of type II diabetes. This
2 Biochemistry Research International
paper summarized the recent advances in understanding ERstress-associated mechanisms in lipid droplet formation andits involvement in type II diabetes.
The paper by B. S. Zha and H. Zhou provided an updatedoverview of ER stress response in lipid metabolism inadipocytes. Adipocytes are one of the major cell typesinvolved in the pathogenesis of the metabolic syndrome.Recent advances in identifying the role of ER stress inregulating lipid metabolism in adipocytes and potentiallinks among ER stress, inflammation, and autophagy werediscussed.
Huiping ZhouKezhong Zhang
Sabina JanciauskieneXiaokun Li
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