Ma HD, Shi L, Li HT, Wang XD, Yang MW. Polycytosine RNA-binding protein 1 regulates osteoblast function via a ferroptosis pathway in type 2 diabetic osteoporosis. World J Diabetes 2024; 15(5): 977-987 [PMID: 38766437 DOI: 10.4239/wjd.v15.i5.977]
Corresponding Author of This Article
Mao-Wei Yang, MD, Chief Doctor, Professor, Department of Orthopedics, The First Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang 110001, Liaoning Province, China. mwyang@cmu.edu.cn
Research Domain of This Article
Orthopedics
Article-Type of This Article
Basic Study
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 Diabetes. May 15, 2024; 15(5): 977-987 Published online May 15, 2024. doi: 10.4239/wjd.v15.i5.977
Polycytosine RNA-binding protein 1 regulates osteoblast function via a ferroptosis pathway in type 2 diabetic osteoporosis
Hong-Dong Ma, Lei Shi, Hai-Tian Li, Xin-Dong Wang, Mao-Wei Yang
Hong-Dong Ma, Lei Shi, Department of Orthopedics, The Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
Hai-Tian Li, Xin-Dong Wang, Mao-Wei Yang, Department of Orthopedics, The First Hospital of China Medical University, Shenyang 110001, Liaoning Province, China
Co-first authors: Hong-Dong Ma and Lei Shi.
Author contributions: Yang MW conceptualized and designed the study; Ma HD and Shi L performed the study and acquired the data, and drafted the manuscript; Li HT and Wang XD analyzed and interpreted the data; Yang MW and Ma HD confirmed the authenticity of the raw data; All authors read and approved the final manuscript.
Supported bythe National Natural Science Foundation of China, No. 81471094 and No. 82202743.
Institutional review board statement: This study was approved by Ethics Committee of Nantong University [approval No. 2023-K185-01].
Conflict-of-interest statement: The authors declare that they have no competing interests.
Data sharing statement: The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.
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: Mao-Wei Yang, MD, Chief Doctor, Professor, Department of Orthopedics, The First Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang 110001, Liaoning Province, China. mwyang@cmu.edu.cn
Received: December 19, 2023 Peer-review started: December 19, 2023 First decision: January 9, 2024 Revised: January 22, 2024 Accepted: March 15, 2024 Article in press: March 15, 2024 Published online: May 15, 2024 Processing time: 143 Days and 10.1 Hours
ARTICLE HIGHLIGHTS
Research background
Type 2 diabetic osteoporosis (T2DOP) has become the most common complication of type 2 diabetes and its incidence has increased annually to seriously threaten human health. Exploring the molecular mechanisms underlying T2DOP is critical for its treatment.
Research motivation
The molecular mechanisms underlying T2DOP are poorly understood.
Research objectives
This study aimed to determine the involvement of ferroptosis and the specific role of polycytosine RNA-binding protein 1 (PCBP1) in the development of T2DOP.
Research methods
A high glucose (HG)-induced in vitro model was established and treated with PCBP1 overexpression lentivirus vectors. The levels of the osteoblast functional proteins osteoprotegerin and osteocalcin, and the ferroptosis-related markers reactive oxygen species and glutathione peroxidase 4 (GPX4) were evaluated.
Research results
HG environment considerably decreased the viability of osteoblasts and enhanced mitochondria atrophy, along with increased PCBP1 and decreased GPX4 expression, whereas treatment with PCBP1 repressed ferroptosis and protected osteoblast function.
Research conclusions
PCBP1 protects osteoblasts from ferroptosis by promoting ferritin expression under the HG stimulation in T2DOP, suggesting the promising therapeutic potential of PCBP1 in T2DOP.
Research perspectives
Our findings revealed a novel regulatory mechanism involved in T2DOP and provided a promising therapeutic approach for clinical use.
