{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nAlthough the initial request sought to summarize the function of ZNF843, none of the provided abstracts mention or describe any role for ZNF843. Rather, the cited studies consistently focus on acyl‐coenzyme A thioesterase 1 (ACOT1), an enzyme that regulates lipid metabolism by hydrolyzing long‐chain acyl-CoAs into free fatty acids and coenzyme A. Notably, ACOT1’s transcription is strongly induced by metabolic regulators such as peroxisome proliferator-activated receptor alpha (PPARα) and hepatocyte nuclear factor 4α (HNF4α), underlining its importance in liver lipid metabolism and its responsiveness to fibrate treatments."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of cardiac function, enhanced ACOT1 expression in cardiomyocytes was shown to ameliorate myocardial dysfunction associated with sepsis. Mechanistically, ACOT1 supports energy production by increasing both glucose utilization and fatty acid oxidation, a process that appears to involve the activation of PPARα/PGC1α signaling pathways. This protective mechanism suggests promising therapeutic potential for conditions where energy deprivation underlies heart dysfunction."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFurthermore, studies in high-fat diet-induced obesity models revealed that the genetic ablation of ACOT1 confers partial protection against weight gain. This effect is associated with an increase in energy expenditure, potentially mediated by mitochondrial uncoupling via upregulation of UCP2, along with a reduction in markers of oxidative stress. These findings collectively emphasize ACOT1’s multifaceted role in metabolic regulation, particularly regarding energy homeostasis and lipid handling under conditions of metabolic stress."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Bikesh Dongol, Yatrik Shah, Insook Kim, et al. "}, {"type": "b", "children": [{"type": "t", "text": "The acyl-CoA thioesterase I is regulated by PPARalpha and HNF4alpha via a distal response element in the promoter."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Lipid Res (2007)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1194/jlr.M700119-JLR200"}], "href": "https://doi.org/10.1194/jlr.M700119-JLR200"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "17485727"}], "href": "https://pubmed.ncbi.nlm.nih.gov/17485727"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Shenglan Yang, Chen Chen, Hong Wang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Protective effects of Acyl-coA thioesterase 1 on diabetic heart via PPARα/PGC1α signaling."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "PLoS One (2012)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1371/journal.pone.0050376"}], "href": "https://doi.org/10.1371/journal.pone.0050376"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "23226270"}], "href": "https://pubmed.ncbi.nlm.nih.gov/23226270"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Congying Xia, Ruolan Dong, Chen Chen, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Cardiomyocyte specific expression of Acyl-coA thioesterase 1 attenuates sepsis induced cardiac dysfunction and mortality."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biochem Biophys Res Commun (2015)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.bbrc.2015.10.078"}], "href": "https://doi.org/10.1016/j.bbrc.2015.10.078"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "26518651"}], "href": "https://pubmed.ncbi.nlm.nih.gov/26518651"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Timothy D Heden, Mallory P Franklin, Christina Dailey, et al. "}, {"type": "b", "children": [{"type": "t", "text": "ACOT1 deficiency attenuates high-fat diet-induced fat mass gain by increasing energy expenditure."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "JCI Insight (2023)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1172/jci.insight.160987"}], "href": "https://doi.org/10.1172/jci.insight.160987"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "37561578"}], "href": "https://pubmed.ncbi.nlm.nih.gov/37561578"}]}]}]}