Yao M, Zhou P, Qin YY, Wang L, Yao DF. Mitochondrial carnitine palmitoyltransferase-II dysfunction: A possible novel mechanism for nonalcoholic fatty liver disease in hepatocarcinogenesis. World J Gastroenterol 2023; 29(12): 1765-1778 [PMID: 37032731 DOI: 10.3748/wjg.v29.i12.1765]
Corresponding Author of This Article
Deng-Fu Yao, MD, PhD, Full Professor, Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, No. 20 West Temple Road, Nantong 226001, Jiangsu Province, China. yaodf@ahnmc.com
Research Domain of This Article
Oncology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Mar 28, 2023; 29(12): 1765-1778 Published online Mar 28, 2023. doi: 10.3748/wjg.v29.i12.1765
Mitochondrial carnitine palmitoyltransferase-II dysfunction: A possible novel mechanism for nonalcoholic fatty liver disease in hepatocarcinogenesis
Min Yao, Ping Zhou, Yan-Yan Qin, Li Wang, Deng-Fu Yao
Min Yao, Department of Medical Immunology, Medical School of Nantong University & Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
Ping Zhou, Yan-Yan Qin, Department of Medical Immunology, Medical School of Nantong University, Nantong 226001, Jiangsu Province, China
Li Wang, Research Center for Intelligent Information Technology, Nantong University, Nantong 226019, Jiangsu Province, China
Deng-Fu Yao, Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
Author contributions: Yao M, Zhou P and Qin YY contributed equally to this work, designed, collected and analyzed the data, prepared the first draft and performed subsequent revisions; Yao DF and Wang L provided critical review; All authors have read and agreed to the published version of the manuscript.
Supported bythe National Natural Science Foundation of China, No. 81873915 and No. 31872738; the Key Plan of Nantong S&T Development, No. MS12020021; and the S&T Program of Medical School of Nantong University, No. TDYX2021010.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Deng-Fu Yao, MD, PhD, Full Professor, Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, No. 20 West Temple Road, Nantong 226001, Jiangsu Province, China. yaodf@ahnmc.com
Received: June 20, 2022 Peer-review started: June 20, 2022 First decision: August 1, 2022 Revised: August 4, 2022 Accepted: March 9, 2023 Article in press: March 9, 2023 Published online: March 28, 2023 Processing time: 281 Days and 7.3 Hours
Core Tip
Core Tip: The complex mechanisms of nonalcoholic fatty liver disease formation are still under identification. Hepatic carnitine palmitoyl transferase-II (CPT-II) on inner mitochondrial membrane regulates long chain fatty acid β-oxidation and this abnormality has had more attention paid to it by basic and clinical research. The sequences of its peptide chain and DNA nucleotides have been identified and the catalytic activity of CPT-II is affected on its gene mutations, deficiency, enzymatic thermal instability, circulating carnitine level and so on. CPT-II dysfunction has been discovered in models of lipid accumulation. Meanwhile, the malignant transformation of hepatocyte-related CD44+ stem T cell activation, high levels of tumor-related biomarkers and abnormal Wnt3a expression as a key signal molecule of the Wnt/β-catenin pathway run parallel to the alterations of hepatocyte pathology.
