{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zang Y"],"funding":["Youth project of Shanghai Municipal Commission of Health and Family Planning","Planned Science Program of the Shanghai University of Traditional Chinese Medicine","Science and Technology Innovation Project of Putuo District Health System","Exploration Program of Putuo Hospital","National Natural Science Foundation of China","Key Medical Discipline Project of Shanghai Municipal Health Bureau"],"pagination":["1453-1464"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7925475"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["48(2)"],"pubmed_abstract":["Loss of podocytes is a hallmark of diabetic nephropathy, and a growing body of evidence indicates that podocytes are susceptible to palmitic acid (PA). We have previously shown that AS-IV inhibited PA-induced podocyte apoptosis by activating sarcoendoplasmic reticulum Ca<sup>2+</sup> ATPase (SERCA), which indicate calcium regulation may involve in the process. Immunofluorescence staining, Western blot and flow cytometry were used to measure the protective efficacy of AS-IV to ameliorate PA-induced ER stress and podocyte apoptosis. Meanwhile, AS-IV inhibited cytochrome c release, decreased mitochondrial membrane potential, accompany with the depletion of endoplasmic reticulum Ca<sup>2+</sup> and elevation of cytosolic and mitochondrial Ca<sup>2+</sup>. Sequestration of cytosolic calcium wit"],"journal":["Molecular biology reports"],"pubmed_title":["Astragaloside IV inhibits palmitic acid-induced apoptosis through regulation of calcium homeostasis in mice podocytes."],"pmcid":["PMC7925475"],"funding_grant_id":["20154Y0133","81403235, 81803921","PTKWWS202001","2020360A","2020LK070","ZK2019A12"],"pubmed_authors":["Shan X","Li Z","Peng W","Zang Y","Liu S","Wang H","Wang Y","Deng W","Cao A","Wang L"],"additional_accession":[]},"is_claimable":false,"name":"Astragaloside IV inhibits palmitic acid-induced apoptosis through regulation of calcium homeostasis in mice podocytes.","description":"Loss of podocytes is a hallmark of diabetic nephropathy, and a growing body of evidence indicates that podocytes are susceptible to palmitic acid (PA). We have previously shown that AS-IV inhibited PA-induced podocyte apoptosis by activating sarcoendoplasmic reticulum Ca<sup>2+</sup> ATPase (SERCA), which indicate calcium regulation may involve in the process. Immunofluorescence staining, Western blot and flow cytometry were used to measure the protective efficacy of AS-IV to ameliorate PA-induced ER stress and podocyte apoptosis. Meanwhile, AS-IV inhibited cytochrome c release, decreased mitochondrial membrane potential, accompany with the depletion of endoplasmic reticulum Ca<sup>2+</sup> and elevation of cytosolic and mitochondrial Ca<sup>2+</sup>. Sequestration of cytosolic calcium wit","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Feb","modification":"2025-04-21T16:58:55.743Z","creation":"2025-04-21T16:58:55.743Z"},"accession":"S-EPMC7925475","cross_references":{"pubmed":["33606151"],"doi":["10.1007/s11033-021-06204-4"]}}