# The role of ferroptosis in osteoporosis: a cellular perspective on osteoblast, osteoclast and osteocyte dysfunction

## TL;DR

This paper explores how a type of cell death called ferroptosis contributes to osteoporosis by affecting bone-forming and bone-resorbing cells.

## Contribution

The paper provides a comprehensive review of how ferroptosis influences osteoblasts, osteoclasts, and osteocytes in osteoporosis.

## Key findings

- Ferroptosis is linked to dysfunction in osteoblasts, osteoclasts, and osteocytes in osteoporosis.
- Aging, estrogen deficiency, and diabetes are factors that influence ferroptosis in bone cells.
- Understanding ferroptosis could lead to new therapeutic strategies for osteoporosis.

## Abstract

Osteoporosis is characterized by an imbalance between bone resorption and bone formation, leading to the loss of both trabecular and cortical bone mass, ultimately resulting in an increased risk of fractures. Osteoporosis represents a major global health burden, predominantly affecting elderly individuals and postmenopausal women. With the continued growth of the aging population, the prevalence of osteoporosis is expected to increase, highlighting the urgent need for more effective therapeutic strategies. Ferroptosis, a recently characterized form of iron-dependent, non-apoptotic cell death, has emerged as an important mechanism contributing to the pathogenesis of osteoporosis. A better understanding of ferroptosis may therefore provide new insights into therapeutic development. This review summarizes current evidence regarding the role of ferroptosis in osteoporosis, with particular focus on its effects on osteoblasts, osteoclasts, and osteocytes, as well as the impact of aging, estrogen deficiency, diabetes, glucocorticoid exposure, and obesity on ferroptosis in osteogenic cells.