Insight of the role of mitochondrial iron homeostasis in insulin resistance
- 1Evidence-Based Nursing Research Laboratory, West China Hospital, Sichuan University/West China School of Nursing, Sichuan University, Chengdu, Sichuan, China
- 2Department of Nursing, West China Hospital, Sichuan University/West China School of Nursing, Sichuan University, Chengdu, Sichuan, China
Abstract
Insulin resistance (IR) is characterized by impaired insulin responsiveness in metabolic tissues, leading to defective glucose disposal, dysregulated lipid metabolism, and compensatory hyperinsulinemia. Mitochondrial iron homeostasis is crucial for cellular metabolism, oxidative phosphorylation (OXPHOS), and redox balance. Dysregulation of mitochondrial iron contributes to IR by impairing electron transport chain (ETC) function, increasing reactive oxygen species (ROS), and disrupting insulin signaling pathways. Excess mitochondrial iron leads to oxidative stress through the Fenton reaction, promoting lipid peroxidation, mitochondrial dysfunction, and inflammation, all of which exacerbate metabolic disorders. Additionally, mitochondrial iron overload affects iron-sulfur (Fe-S) cluster biosynthesis, mitochondrial dynamics, and energy metabolism, further impairing glucose homeostasis. Emerging evidence suggests that mitochondrial iron dysregulation plays a pivotal role in the pathogenesis of type 2 diabetes mellitus (T2DM) and metabolic syndrome. Future research should focus on the molecular mechanisms governing mitochondrial iron transport and utilization, as well as its interaction with key metabolic pathways, to better understand its role in disease progression and potential therapeutic implications.
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BibTeX
@article{dong2026insight,
title = {{Insight of the role of mitochondrial iron homeostasis in insulin resistance}},
author = {Zhanchen Dong and Yan Jiang},
journal = {PeerJ},
year = {2026},
month = nov,
doi = {10.7717/peerj.21873},
url = {https://peerj.com/articles/21873},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Insight of the role of mitochondrial iron homeostasis in insulin resistance
AU - Zhanchen Dong
AU - Yan Jiang
PY - 2026
DA - 2026/11/02
JO - PeerJ
DO - 10.7717/peerj.21873
UR - https://peerj.com/articles/21873
AB - Insulin resistance (IR) is characterized by impaired insulin responsiveness in metabolic tissues, leading to defective glucose disposal, dysregulated lipid metabolism, and compensatory hyperinsulinemia. Mitochondrial iron homeostasis is crucial for cellular metabolism, oxidative phosphorylation (OXPHOS), and redox balance. Dysregulation of mitochondrial iron contributes to IR by impairing electron transport chain (ETC) function, increasing reactive oxygen species (ROS), and disrupting insulin signaling pathways. Excess mitochondrial iron leads to oxidative stress through the Fenton reaction, promoting lipid peroxidation, mitochondrial dysfunction, and inflammation, all of which exacerbate metabolic disorders. Additionally, mitochondrial iron overload affects iron-sulfur (Fe-S) cluster biosynthesis, mitochondrial dynamics, and energy metabolism, further impairing glucose homeostasis. Emerging evidence suggests that mitochondrial iron dysregulation plays a pivotal role in the pathogenesis of type 2 diabetes mellitus (T2DM) and metabolic syndrome. Future research should focus on the molecular mechanisms governing mitochondrial iron transport and utilization, as well as its interaction with key metabolic pathways, to better understand its role in disease progression and potential therapeutic implications.
SN - 2167-8359
ER -