{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"Research Square"}],"indexed":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T17:14:38Z","timestamp":1783444478340,"version":"3.54.6"},"posted":{"date-parts":[[2026,5,19]]},"group-title":"In Review","reference-count":41,"publisher":"Springer Science and Business Media LLC","license":[{"start":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T00:00:00Z","timestamp":1779148800000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,4,14]]},"abstract":"<title>Abstract<\/title>\n                <p>Background\n Acute kidney injury (AKI) frequently causes remote organ injury including hepatic steatosis, yet whether lipid accumulation reflects increased synthesis or impaired clearance has not been resolved.\nMethods\n We used a murine ischemia-reperfusion AKI model. Unbiased liver proteomics was performed at 24 hours after reperfusion, and dysregulated pathways were identified by Gene Set Enrichment Analysis. Results were validated by Western blotting, qPCR, and immunohistochemistry. These findings were complemented by retrospective analysis of two ICU databases (MIMIC-IV and eICU-CRD).\nResults\n AKI significantly increased serum ALT and AST and induced hepatic lipid accumulation. Proteomic analysis revealed that key lipogenic enzymes (Scd1, Fasn, Acly, Acaca) were uniformly suppressed rather than upregulated. Proteins essential for VLDL assembly (ApoB, MTTP, ApoE) were significantly downregulated. Plasma triglycerides were decreased while liver triglycerides were increased, consistent with impaired hepatic lipid export. As in renal tubular cells, AKI also disrupted ER protein folding homeostasis in the liver, triggering ER stress. This was evidenced by upregulated levels of the ER chaperone GRP78, increased XBP1 splicing indicative of UPR activation, and elevated expression of the ER stress-induced pro-apoptotic transcription factor CHOP, suggesting that prolonged ER stress may also promote hepatocyte cell death. TLR4\/MyD88 signaling was activated, yet inflammatory cytokines were paradoxically reduced, accompanied by Kupffer cell depletion (decreased F4\/80) and monocyte infiltration (increased CD68). In 6,996 propensity-matched ICU patients (MIMIC-IV), AKI independently increased the risk of clinically significant liver injury 4-fold (adjusted OR\u2009=\u20094.41). Analysis of 22,727 patients across 208 hospitals (eICU-CRD) identified a lipid dissociation pattern: elevated triglycerides alongside decreased total cholesterol, HDL, and LDL, with dose-dependent scaling across KDIGO stages.\nConclusions\n These data support ER stress-mediated impairment of VLDL export as a primary driver of AKI-induced hepatic steatosis. Clinical validation across two independent ICU databases identifies a dual metabolic insult: enhanced peripheral lipid delivery compounds impaired hepatic export, amplifying hepatic lipid retention. ER stress and lipid export machinery represent potential therapeutic targets for AKI-associated liver injury.<\/p>","DOI":"10.21203\/rs.3.rs-9409706\/v1","type":"posted-content","created":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T09:21:13Z","timestamp":1779182473000},"source":"Crossref","is-referenced-by-count":0,"title":["ER Stress-Mediated Impairment of Hepatic Lipid Export Drives Steatosis in AKI-Induced Remote Liver Injury"],"prefix":"10.21203","author":[{"given":"Minghua","family":"Li","sequence":"first","affiliation":[{"name":"University of South Florida (USF)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Runze","family":"Ni","sequence":"additional","affiliation":[{"name":"University of South Florida (USF)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristof","family":"Williams","sequence":"additional","affiliation":[{"name":"University of South Florida (USF)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miriame","family":"Melaika","sequence":"additional","affiliation":[{"name":"University of South Florida (USF)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lucas Eli","family":"Sun","sequence":"additional","affiliation":[{"name":"University of South Florida (USF)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liying","family":"Fu","sequence":"additional","affiliation":[{"name":"Mayo Clinic"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vijay","family":"Subramanian","sequence":"additional","affiliation":[{"name":"Tampa General Hospital"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kiran","family":"Dhanireddy","sequence":"additional","affiliation":[{"name":"Tampa General Hospital"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruisheng","family":"Liu","sequence":"additional","affiliation":[{"name":"University of South Florida (USF)"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","reference":[{"key":"ref1","doi-asserted-by":"publisher","first-page":"1218","DOI":"10.1093\/ndt\/gfaa297","article-title":"Renohepatic crosstalk: a review of the effects of acute kidney injury on the liver","volume":"37","author":"Bonavia A","year":"2022","unstructured":"Bonavia, A. & Stiles, N. 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Gastroenterol."},{"key":"ref8","doi-asserted-by":"publisher","first-page":"23","DOI":"10.1016\/j.cld.2017.08.007","article-title":"Pathophysiology of Nonalcoholic Fatty Liver Disease\/Nonalcoholic Steatohepatitis","volume":"22","author":"Manne V","year":"2018","unstructured":"Manne, V., Handa, P. & Kowdley, K. V. Pathophysiology of Nonalcoholic Fatty Liver Disease\/Nonalcoholic Steatohepatitis. Clin. Liver Dis. 22, 23\u201337. 10.1016\/j.cld.2017.08.007 (2018).","journal-title":"Clin. Liver Dis."},{"key":"ref9","doi-asserted-by":"publisher","first-page":"1664","DOI":"10.3748\/wjg.v22.i4.1664","article-title":"Mechanisms of intrahepatic triglyceride accumulation","volume":"22","author":"Ress C","year":"2016","unstructured":"Ress, C. & Kaser, S. Mechanisms of intrahepatic triglyceride accumulation. World J. Gastroenterol. 22, 1664\u20131673. 10.3748\/wjg.v22.i4.1664 (2016).","journal-title":"World J. Gastroenterol."},{"key":"ref10","doi-asserted-by":"publisher","first-page":"1134","DOI":"10.3389\/fphar.2019.01134","article-title":"Protective Effect of Patchouli Alcohol Against High-Fat Diet Induced Hepatic Steatosis by Alleviating Endoplasmic Reticulum Stress and Regulating VLDL Metabolism in Rats","volume":"10","author":"Wu X","year":"2019","unstructured":"Wu, X. et al. Protective Effect of Patchouli Alcohol Against High-Fat Diet Induced Hepatic Steatosis by Alleviating Endoplasmic Reticulum Stress and Regulating VLDL Metabolism in Rats. Front. Pharmacol. 10, 1134. 10.3389\/fphar.2019.01134 (2019).","journal-title":"Front. Pharmacol."},{"key":"ref11","doi-asserted-by":"publisher","DOI":"10.3390\/ijms19082291","article-title":"Induction of Liver Steatosis in BAP31-Deficient Mice Burdened with Tunicamycin-Induced Endoplasmic Reticulum Stress","volume":"19","author":"Wu Z","year":"2018","unstructured":"Wu, Z., Yang, F., Jiang, S., Sun, X. & Xu, J. 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Physiol. 319, F304\u2013F311. 10.1152\/ajprenal.00017.2020 (2020).","journal-title":"Am. J. Physiol. Ren. Physiol."},{"key":"ref18","doi-asserted-by":"publisher","first-page":"e215","DOI":"10.1161\/01.CIR.101.23.e215","article-title":"PhysioBank, PhysioToolkit, and PhysioNet: Components of a new research resource for complex physiologic signals","volume":"101","author":"Goldberger AL","year":"2000","unstructured":"Goldberger, A. L. et al. PhysioBank, PhysioToolkit, and PhysioNet: Components of a new research resource for complex physiologic signals. Circulation 101, e215\u2013e220. 10.1161\/01.CIR.101.23.e215 (2000).","journal-title":"Circulation"},{"key":"ref19","author":"Johnson A","year":"2024","unstructured":"Johnson, A. et al. (PhysioNet, (2024)."},{"key":"ref20","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1038\/s41597-022-01899-x","article-title":"MIMIC-IV, a freely accessible electronic health record dataset","volume":"10","author":"Johnson AEW","year":"2023","unstructured":"Johnson, A. E. W. et al. MIMIC-IV, a freely accessible electronic health record dataset. Sci. Data. 10, 1. 10.1038\/s41597-022-01899-x (2023).","journal-title":"Sci. Data"},{"key":"ref21","author":"Pollard T","year":"2019","unstructured":"Pollard, T. et al. (PhysioNet, (2019)."},{"key":"ref22","doi-asserted-by":"publisher","first-page":"180178","DOI":"10.1038\/sdata.2018.178","article-title":"The eICU Collaborative Research Database, a freely available multi-center database for critical care research","volume":"5","author":"Pollard TJ","year":"2018","unstructured":"Pollard, T. J. et al. The eICU Collaborative Research Database, a freely available multi-center database for critical care research. Sci. Data. 5, 180178. 10.1038\/sdata.2018.178 (2018).","journal-title":"Sci. Data"},{"key":"ref23","doi-asserted-by":"publisher","first-page":"D672","DOI":"10.1093\/nar\/gkae909","article-title":"KEGG: biological systems database as a model of the real world","volume":"53","author":"Kanehisa M","year":"2025","unstructured":"Kanehisa, M., Furumichi, M., Sato, Y., Matsuura, Y. & Ishiguro-Watanabe, M. KEGG: biological systems database as a model of the real world. Nucleic Acids Res. 53, D672\u2013D677. 10.1093\/nar\/gkae909 (2025).","journal-title":"Nucleic Acids Res."},{"key":"ref24","doi-asserted-by":"publisher","first-page":"27","DOI":"10.1093\/nar\/28.1.27","article-title":"KEGG: kyoto encyclopedia of genes and genomes","volume":"28","author":"Kanehisa M","year":"2000","unstructured":"Kanehisa, M. & Goto, S. KEGG: kyoto encyclopedia of genes and genomes. Nucleic Acids Res. 28, 27\u201330. 10.1093\/nar\/28.1.27 (2000).","journal-title":"Nucleic Acids Res."},{"key":"ref25","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1002\/cphy.c170012","article-title":"Triglyceride Metabolism in the Liver","volume":"8","author":"Alves-Bezerra M","year":"2017","unstructured":"Alves-Bezerra, M. & Cohen, D. E. Triglyceride Metabolism in the Liver. Compr. Physiol. 8, 1\u20138. 10.1002\/cphy.c170012 (2017).","journal-title":"Compr. Physiol."},{"key":"ref26","doi-asserted-by":"publisher","first-page":"1347","DOI":"10.1042\/CS20220572","article-title":"Molecular mechanisms of metabolic associated fatty liver disease (MAFLD): functional analysis of lipid metabolism pathways","volume":"136","author":"Badmus OO","year":"2022","unstructured":"Badmus, O. O., Hillhouse, S. A., Anderson, C. D., Hinds, T. D. & Stec, D. E. Molecular mechanisms of metabolic associated fatty liver disease (MAFLD): functional analysis of lipid metabolism pathways. Clin. Sci. (Lond). 136, 1347\u20131366. 10.1042\/CS20220572 (2022).","journal-title":"Clin. Sci. (Lond)"},{"key":"ref27","doi-asserted-by":"publisher","first-page":"239","DOI":"10.1124\/mol.117.111146","article-title":"Activation of Constitutive Androstane Receptor Ameliorates Renal Ischemia-Reperfusion-Induced Kidney and Liver Injury","volume":"93","author":"Choi YJ","year":"2018","unstructured":"Choi, Y. J. et al. Activation of Constitutive Androstane Receptor Ameliorates Renal Ischemia-Reperfusion-Induced Kidney and Liver Injury. Mol. Pharmacol. 93, 239\u2013250. 10.1124\/mol.117.111146 (2018).","journal-title":"Mol. Pharmacol."},{"key":"ref28","doi-asserted-by":"publisher","first-page":"84","DOI":"10.1186\/s40635-023-00570-y","article-title":"Impact of critical illness on cholesterol and fatty acids: insights into pathophysiology and therapeutic targets","volume":"11","author":"Lauwers C","year":"2023","unstructured":"Lauwers, C., De Bruyn, L. & Langouche, L. Impact of critical illness on cholesterol and fatty acids: insights into pathophysiology and therapeutic targets. Intensive Care Med. Exp. 11, 84. 10.1186\/s40635-023-00570-y (2023).","journal-title":"Intensive Care Med. Exp."},{"key":"ref29","doi-asserted-by":"publisher","first-page":"1169","DOI":"10.1194\/jlr.R300019-JLR200","article-title":"Effects of infection and inflammation on lipid and lipoprotein metabolism: mechanisms and consequences to the host","volume":"45","author":"Khovidhunkit W","year":"2004","unstructured":"Khovidhunkit, W. et al. Effects of infection and inflammation on lipid and lipoprotein metabolism: mechanisms and consequences to the host. J. Lipid Res. 45, 1169\u20131196. 10.1194\/jlr.R300019-JLR200 (2004).","journal-title":"J. Lipid Res."},{"key":"ref30","doi-asserted-by":"publisher","DOI":"10.3390\/jcm10081693","article-title":"Lipid and Lipoprotein Dysregulation in Sepsis: Clinical and Mechanistic Insights into Chronic Critical Illness","volume":"10","author":"Barker G","year":"2021","unstructured":"Barker, G. et al. Lipid and Lipoprotein Dysregulation in Sepsis: Clinical and Mechanistic Insights into Chronic Critical Illness. J. Clin. Med. 10 10.3390\/jcm10081693 (2021).","journal-title":"J. Clin. Med."},{"key":"ref31","doi-asserted-by":"publisher","first-page":"453","DOI":"10.1186\/s13054-025-05702-2","article-title":"High-density lipoprotein: a biomarker and therapeutic target in sepsis","volume":"29","author":"Li M","year":"2025","unstructured":"Li, M. et al. High-density lipoprotein: a biomarker and therapeutic target in sepsis. Crit. Care. 29, 453. 10.1186\/s13054-025-05702-2 (2025).","journal-title":"Crit. Care"},{"key":"ref32","doi-asserted-by":"publisher","first-page":"17377","DOI":"10.1074\/jbc.R100068200","article-title":"N. Complexity in the secretory pathway: the assembly and secretion of apolipoprotein B-containing lipoproteins","volume":"277","author":"Fisher EA","year":"2002","unstructured":"Fisher, E. A. & Ginsberg, H. N. Complexity in the secretory pathway: the assembly and secretion of apolipoprotein B-containing lipoproteins. J. Biol. Chem. 277, 17377\u201317380. 10.1074\/jbc.R100068200 (2002).","journal-title":"J. Biol. Chem."},{"key":"ref33","doi-asserted-by":"publisher","first-page":"316","DOI":"10.1172\/JCI32752","article-title":"Inhibition of apolipoprotein B100 secretion by lipid-induced hepatic endoplasmic reticulum stress in rodents","volume":"118","author":"Ota T","year":"2008","unstructured":"Ota, T., Gayet, C. & Ginsberg, H. N. Inhibition of apolipoprotein B100 secretion by lipid-induced hepatic endoplasmic reticulum stress in rodents. J. Clin. Invest. 118, 316\u2013332. 10.1172\/JCI32752 (2008).","journal-title":"J. Clin. Invest."},{"key":"ref34","doi-asserted-by":"publisher","first-page":"3852","DOI":"10.1172\/JCI86028","article-title":"Inhibition of apolipoprotein B synthesis stimulates endoplasmic reticulum autophagy that prevents steatosis","volume":"126","author":"Conlon DM","year":"2016","unstructured":"Conlon, D. M. et al. Inhibition of apolipoprotein B synthesis stimulates endoplasmic reticulum autophagy that prevents steatosis. J. Clin. Invest. 126, 3852\u20133867. 10.1172\/JCI86028 (2016).","journal-title":"J. Clin. Invest."},{"key":"ref35","first-page":"224","article-title":"Exposure to fine airborne particulate matter induces macrophage infiltration, unfolded protein response, and lipid deposition in white adipose tissue","volume":"5","author":"Mendez R","year":"2013","unstructured":"Mendez, R. et al. Exposure to fine airborne particulate matter induces macrophage infiltration, unfolded protein response, and lipid deposition in white adipose tissue. Am. J. Transl Res. 5, 224\u2013234 (2013).","journal-title":"Am. J. Transl Res."},{"key":"ref36","doi-asserted-by":"publisher","first-page":"786","DOI":"10.1016\/j.imbio.2017.01.003","article-title":"Hepatic interleukin-6 production is maintained during endotoxin tolerance and facilitates lipid accumulation","volume":"222","author":"Dembek A","year":"2017","unstructured":"Dembek, A. et al. Hepatic interleukin-6 production is maintained during endotoxin tolerance and facilitates lipid accumulation. Immunobiology 222, 786\u2013796. 10.1016\/j.imbio.2017.01.003 (2017).","journal-title":"Immunobiology"},{"key":"ref37","doi-asserted-by":"publisher","DOI":"10.3390\/life12030354","article-title":"Taurine Ameliorates Tunicamycin-Induced Liver Injury by Disrupting the Vicious Cycle between Oxidative Stress and Endoplasmic Reticulum Stress","volume":"12","author":"Kim SH","year":"2022","unstructured":"Kim, S. H., Seo, H., Kwon, D., Yuk, D. Y. & Jung, Y. S. Taurine Ameliorates Tunicamycin-Induced Liver Injury by Disrupting the Vicious Cycle between Oxidative Stress and Endoplasmic Reticulum Stress. Life (Basel). 12 10.3390\/life12030354 (2022).","journal-title":"Life (Basel)"},{"key":"ref38","doi-asserted-by":"publisher","first-page":"105218","DOI":"10.1016\/j.phrs.2020.105218","article-title":"Endoplasmic reticulum stress and protein degradation in chronic liver disease","volume":"161","author":"Xia SW","year":"2020","unstructured":"Xia, S. W. et al. Endoplasmic reticulum stress and protein degradation in chronic liver disease. Pharmacol. Res. 161, 105218. 10.1016\/j.phrs.2020.105218 (2020).","journal-title":"Pharmacol. Res."},{"key":"ref39","doi-asserted-by":"publisher","first-page":"10874","DOI":"10.7150\/thno.47037","article-title":"Dysfunction of estrogen-related receptor alpha-dependent hepatic VLDL secretion contributes to sex disparity in NAFLD\/NASH development","volume":"10","author":"Yang M","year":"2020","unstructured":"Yang, M. et al. Dysfunction of estrogen-related receptor alpha-dependent hepatic VLDL secretion contributes to sex disparity in NAFLD\/NASH development. 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