Evidence map›Paper›PMID 33594527›Full record

ArticleBiological trace element research2022

Mitochondrial Ferritin Deficiency Promotes Osteoblastic Ferroptosis Via Mitophagy in Type 2 Diabetic Osteoporosis.

XinDong Wang, HongDong Ma, Jun Sun, TianYu Zheng, Peng Zhao, HaiTian Li, MaoWei Yang

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Article in Biological trace element research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
8.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

101 citing papers in PubMed, 140 citations in OpenAlex.

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41 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

XinDong Wang *Department of Orthopedics, The First Hospital of China Medical University, 155 North Nanjing Street, Shenyang, 110001, Liaoning, China.
HongDong Ma *Department of Orthopedics, The First Hospital of China Medical University, 155 North Nanjing Street, Shenyang, 110001, Liaoning, China.
Jun SunDepartment of Orthopedics, The Third Hospital of Jinzhou Medical University, Jinzhou, Liaoning, China.
TianYu ZhengThe VIP Department, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Diseases, Shenyang, Liaoning, China.
Peng ZhaoDepartment of Orthopedics, The First Hospital of China Medical University, 155 North Nanjing Street, Shenyang, 110001, Liaoning, China.
HaiTian LiDepartment of Orthopedics, The First Hospital of China Medical University, 155 North Nanjing Street, Shenyang, 110001, Liaoning, China.
MaoWei YangDepartment of Orthopedics, The First Hospital of China Medical University, 155 North Nanjing Street, Shenyang, 110001, Liaoning, China. mwyang@cmu.edu.cn.ORCID http://orcid.org/0000-0003-4304-7661
First Hospital of China Medical University · CNChina Medical University · CNJinzhou Medical University · CN

Funding

National Natural Science Foundation of China 81471094
6 · The paper itself

Abstract

The incidence of type 2 diabetic osteoporosis (T2DOP), which seriously threatens elderly people's health, is rapidly increasing in recent years. However, the specific mechanism of the T2DOP is still unclear. Studies have shown the relationship between iron overload and T2DOP. Mitochondrial ferritin (FtMt) is a protein that stores iron ions and intercepts toxic ferrous ions in cells mitochondria. Ferroptosis, an iron-dependent cell injured way, may be related to the pathogenesis of T2DOP. In this study, we intend to elucidate the effect of FtMt on ferroptosis in osteoblasts and explain the possible mechanism. We first detected the occurrence of ferroptosis in bone tissue and the expression of FtMt after inducing T2DOP rat model. Then we used hFOB1.19 cells to study the influence of high glucose on FtMt, ferroptosis, and osteogenic function of osteoblasts. Then we observed the effect of FtMt on ferroptosis and osteoblast function by lentiviral silencing and overexpression of FtMt. We found ferroptosis in T2DOP rats bone. Overexpression of FtMt reduced osteoblastic ferroptosis under high glucose condition while silent FtMt induced mitophagy through ROS / PINK1/Parkin pathway. Then we found increased ferroptosis in osteoblasts after activating mitophagy by carbonyl cyanide-m-chlorophenyl-hydrazine (CCCP, a mitophagy agonist). Our study demonstrated that FtMt inhibited the occurrence of ferroptosis in osteoblasts by reducing oxidative stress caused by excess ferrous ions, and FtMt deficiency induced mitophagy in the pathogenesis of T2DOP. This study suggested that FtMt might serve as a potential target for T2DOP therapy.

Indexed as

Diabetes Mellitus, Type 2FerroptosisOsteoporosisAnimalsFerritinsMitochondrial ProteinsMitophagyRatsReactive Oxygen SpeciesUbiquitin-Protein LigasesFerritinsmitochondrial ferritin, humanMitochondrial ProteinsReactive Oxygen SpeciesUbiquitin-Protein LigasesFerroptosisMitochondrial ferritinMitophagyOsteoblastReactive oxygen speciesType 2 diabetic osteoporosis

Identifiers

PMID33594527
OpenAlexW3132686663

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.