{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yang Y"],"funding":["National Natural Science Foundation of China","Natural Science Foundation of Beijing of China","the State Key Laboratory of Proteomics"],"pagination":["13325"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9658083"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(21)"],"pubmed_abstract":["Hepassocin (HPS) is a hepatokine that has multiple proposed physiological functions. Some of the biological processes in which it is involved are closely related to endoplasmic reticulum (ER) stress, but the role of HPS in the regulation of ER stress remains unclear. Here, we demonstrated that <i>HPS</i> transcription is induced by the protein kinase RNA-like ER kinase (PERK)/activating transcription factor 4 (ATF4) cascade upon ER stress in hepatocytes. Additionally, fasting/refeeding also induced HPS expression in mice liver. The loss of HPS sensitizes hepatocytes to ER stress-related cytotoxicity in vitro, whereas HPS treatment altered these phenotypes. HPS deficiency exacerbates fasting/refeeding-induced ER stress in vivo. The preliminary administration of HPS ameliorates liver steatos"],"journal":["International journal of molecular sciences"],"pubmed_title":["Protective Role of Hepassocin against Hepatic Endoplasmic Reticulum Stress in Mice."],"pmcid":["PMC9658083"],"funding_grant_id":["SKLP-K201404","82070596","7182124"],"pubmed_authors":["Yang X","Dong D","Yang Y","Wang P","Yu M","Xiang S","Yao S","Wan Y","Chen H","Wang X"],"additional_accession":[]},"is_claimable":false,"name":"Protective Role of Hepassocin against Hepatic Endoplasmic Reticulum Stress in Mice.","description":"Hepassocin (HPS) is a hepatokine that has multiple proposed physiological functions. Some of the biological processes in which it is involved are closely related to endoplasmic reticulum (ER) stress, but the role of HPS in the regulation of ER stress remains unclear. Here, we demonstrated that <i>HPS</i> transcription is induced by the protein kinase RNA-like ER kinase (PERK)/activating transcription factor 4 (ATF4) cascade upon ER stress in hepatocytes. Additionally, fasting/refeeding also induced HPS expression in mice liver. The loss of HPS sensitizes hepatocytes to ER stress-related cytotoxicity in vitro, whereas HPS treatment altered these phenotypes. HPS deficiency exacerbates fasting/refeeding-induced ER stress in vivo. The preliminary administration of HPS ameliorates liver steatos","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Nov","modification":"2025-04-25T23:16:53.343Z","creation":"2025-04-25T23:16:53.343Z"},"accession":"S-EPMC9658083","cross_references":{"pubmed":["36362113"],"doi":["10.3390/ijms232113325"]}}