Prevention and regression of megamitochondria and steatosis by blocking mitochondrial fusion in the liver
Miho Iijima,سلوى محمد عمار +1 more
TLDR
In this article , gene knockout of OPA1, a mitochondrial dynamin-related GTPase that mediates mitochondrial fusion, prevents megamitochondria formation and liver damage in a NASH mouse model induced by a methionine-choline-deficient (MCD) diet.About:
This article is published in iScience.The article was published on 2022-04-01 and is currently open access. It has received 11 citations till now. The article focuses on the topics: Steatohepatitis & Fatty liver.read more
Citations
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Journal ArticleDOI
Mitochondrial alterations in fatty liver diseases.
Bernard Fromenty,Michael Roden +1 more
TL;DR: A review of the current knowledge on hepatic mitochondria with a focus on fatty liver diseases linked to obesity, type 2 diabetes and xenobiotics is presented in this article , which highlights the need to better understand their mutual interaction and potentiation in disease progression.
Posted ContentDOI
Opa1 and Drp1 reciprocally regulate cristae morphology, ETC function, and NAD+ regeneration in KRas-mutant lung adenocarcinoma
Dane Sessions,Kee-Beom Kim,Jennifer A. Kashatus,Nikolas Churchill,Kwon Sik Park,Marty W. Mayo,Hiromi Sesaki,David F. Kashatus +7 more
TL;DR: The results support a model in which mitochondrial fission events disrupt cristae structure and tumor cells with hyperactive fission activity require Opa1 activity to maintain ETC function.
Journal ArticleDOI
Opa1 and Drp1 reciprocally regulate cristae morphology, ETC function, and NAD+ regeneration in KRas-mutant lung adenocarcinoma
TL;DR: In this article , the role of mitochondrial dynamics in other Ras-driven malignancies is poorly defined, but it is shown that in vitro and in vivo growth of KRas-driven lung adenocarcinoma is unaffected by deletion of Drp1 but is inhibited by the deletion of Opa1, the GTPase that regulates inner membrane fusion and proper cristae morphology.
Journal ArticleDOI
Linking nutrient sensing, mitochondrial function, and PRR immune cell signaling in liver disease.
Claudia Kemper,Michael N. Sack +1 more
TL;DR: In this article , the authors hypothesize that altered mitochondrial function, classic PRR signaling and complement activation in response to nutrient overload together play an integrated role across the immune cell landscape, leading to liver inflammation and NASH progression.
Journal ArticleDOI
From Non-Alcoholic Fatty Liver to Hepatocellular Carcinoma: A Story of (Mal)Adapted Mitochondria
TL;DR: In this paper , a review summarizes evidence linking mitochondrial dysfunction with NAFLD pathophysiology, discriminating it in different disease stages (simple steatosis, steatohepatitis, liver fibrosis, cirrhosis, and hepatocellular carcinoma).
References
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Design and validation of a histological scoring system for nonalcoholic fatty liver disease
David E. Kleiner,Elizabeth M. Brunt,Mark L. Van Natta,Cynthia Behling,Melissa J. Contos,Oscar W. Cummings,Linda D. Ferrell,Yao Chang Liu,Michael Torbenson,Aynur Unalp-Arida,Matthew M. Yeh,Arthur J. McCullough,Arun J. Sanyal +12 more
TL;DR: A strong scoring system and NAS for NAFLD and NASH with reasonable inter‐rater reproducibility that should be useful for studies of both adults and children with any degree ofNAFLD are presented.
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Mitofusin 2 tethers endoplasmic reticulum to mitochondria
TL;DR: It is shown that mitofusin 2, a mitochondrial dynamin-related protein mutated in the inherited motor neuropathy Charcot–Marie–Tooth type IIa, is enriched at the ER–mitochondria interface, and that it tethers ER to mitochondria, a juxtaposition required for efficient mitochondrial Ca2+ uptake.
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Modeling the epidemic of nonalcoholic fatty liver disease demonstrates an exponential increase in burden of disease
TL;DR: With continued high rates of adult obesity and DM along with an aging population, NAFLD‐related liver disease and mortality will increase in the United States and strategies to slow the growth ofNAFLD cases and therapeutic options are necessary to mitigate disease burden.
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Dual roles for glucokinase in glucose homeostasis as determined by liver and pancreatic beta cell-specific gene knock-outs using Cre recombinase.
Catherine Postic,Masakazu Shiota,Kevin D. Niswender,T. L. Jetton,Yeujin Chen,J. M. Moates,Kathy D. Shelton,Jill Lindner,Alan D. Cherrington,Mark A. Magnuson +9 more
TL;DR: These studies indicate that deficiencies in both β cell and hepatic GK contribute to the hyperglycemia of MODY-2, and suggest that heterozygous null for GK, either globally or just in the β cell, survive but are moderately hyperglycemic.
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Efficient Reduction of Target RNAs by Small Interfering RNA and RNase H-dependent Antisense Agents: A COMPARATIVE ANALYSIS *
Timothy A. Vickers,Seongjoon Koo,C. Frank Bennett,Stanley T. Crooke,Nicholas M. Dean,Brenda F. Baker +5 more
TL;DR: In this paper, a comparative study of optimized antisense oligonucleotides designed to work by an RNA interference mechanism to oligon nucleotide-dependent mechanisms in human cells was performed and the potency, maximal effectiveness, duration of action, and sequence specificity of optimized RNase H-dependent oligonuclotide and small interfering RNA (siRNA) oligoneucleotide duplexes were evaluated and found to be comparable.
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