Excessive Ca2+-dependent ER-mitochondrial contact stabilization by EFHD1 drives liver injury.

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Title: Excessive Ca2+-dependent ER-mitochondrial contact stabilization by EFHD1 drives liver injury.
Authors: Eberhardt DR; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Rekate EC; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Masini YB; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Duron HE; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Mollinedo D; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Velarde AM; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Stucki D; Department of Internal Medicine, Division of Nephrology and Hypertension, University of Utah, Salt Lake City, UT., Price T; Department of Internal Medicine, Division of Nephrology and Hypertension, University of Utah, Salt Lake City, UT., Lee SHJ; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Balderas E; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Rai NK; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Bratt AR; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Balynas AM; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Stubben CJ; Bioinformatics Shared Resource, Huntsman Cancer Institute, Salt Lake City, UT., Bia R; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Maity S; Thermo Fisher Scientific, San Jose, CA., Hartel N; Thermo Fisher Scientific, San Jose, CA., Yin X; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Corbin A; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Kumari A; Department of Pharmacology and Physiology, University of Maryland School of Medicine, Baltimore, MD., Nguyen DM; Department of Pharmacology and Physiology, University of Maryland School of Medicine, Baltimore, MD., Shimura D; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Nguyen VD; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT., Vinod V; Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT., Chowdhury KH; Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT., Verdeguer F; InSphero AG, Schlieren, Switzerland., Zvick J; InSphero AG, Schlieren, Switzerland., Mimche PN; Department of Dermatology, Indiana University School of Medicine, Indianapolis, IN., Boudina S; Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT., Drakos SG; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT.; Department of Internal Medicine, Division of Cardiovascular Medicine, University of Utah, Salt Lake City, UT., Aromolaran AS; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT.; Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT.; Department of Surgery, Division of Cardiothoracic Surgery, University of Utah, Salt Lake City, UT.; Departments of Biochemistry and Biomedical Engineering, University of Utah, Salt Lake City, UT., Franklin S; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT.; Department of Internal Medicine, Division of Cardiovascular Medicine, University of Utah, Salt Lake City, UT., Garg V; Department of Pharmacology and Physiology, University of Maryland School of Medicine, Baltimore, MD., Shaw RM; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT.; Department of Internal Medicine, Division of Cardiovascular Medicine, University of Utah, Salt Lake City, UT., Holland WL; Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT., Summers SA; Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT., Pezzolesi MG; Department of Internal Medicine, Division of Nephrology and Hypertension, University of Utah, Salt Lake City, UT.; Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT.; Department of Human Genetics, University of Utah, Salt Lake City, UT., Rutter J; Howard Hughes Medical Institute, Department of Biochemistry, University of Utah, Salt Lake City, UT., Evason KJ; Department of Pathology and Huntsman Cancer Institute, University of Utah, Salt Lake City, UT., Chaudhuri D; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT.; Department of Internal Medicine, Division of Cardiovascular Medicine, University of Utah, Salt Lake City, UT.; Departments of Biochemistry and Biomedical Engineering, University of Utah, Salt Lake City, UT.
Source: BioRxiv : the preprint server for biology [bioRxiv] 2026 Feb 16. Date of Electronic Publication: 2026 Feb 16.
Publication Type: Journal Article; Preprint
Journal Info: Country of Publication: United States NLM ID: 101680187 Publication Model: Electronic Cited Medium: Internet ISSN: 2692-8205 (Electronic) Linking ISSN: 26928205 NLM ISO Abbreviation: bioRxiv Subsets: PubMed not MEDLINE
Database: MEDLINE Ultimate
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PubType: Academic Journal
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  Data: Excessive Ca<superscript>2+</superscript>-dependent ER-mitochondrial contact stabilization by EFHD1 drives liver injury.
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