Abstract:Reduced bone mass and degeneration of the microarchitecture of bone tissue are
the hallmarks of osteoporosis, a bone metabolic disease that increases skeletal
fragility and fracture susceptibility. Osteoporosis is primarily caused by
unbalanced bone remodeling, in which bone synthesis is outpaced by bone
resorption caused by osteoclasts. Along with the bone-building vitamins calcium
and vitamin D, typical medications for treating osteoporosis include
bisphosphonates and calcitonin. The present therapies effectively stop
osteoclast activation that is too high, however they come with varying degrees
of negative effects. Numerous factors can contribute to osteoporosis, which is
characterized by a loss of bone mass and density due to the deterioration of the
bone’s microstructure, which makes the bone more fragile. As a result,
it is a systemic bone condition that makes patients more likely to fracture.
Interest in the function of ferroptosis in the pathophysiology of osteoporosis
is developing. In this review, we go through the shape of the cell, the
fundamental mechanisms of ferroptosis, the relationship between osteoclasts and
osteoblasts, the association between ferroptosis and diabetic osteoporosis,
steroid-induced osteoporosis, and the relationship between ferroptosis and
postmenopausal osteoporosis. The functions of ferroptosis and osteoporosis in
cellular function, signaling cascades, pharmacological inhibition, and gene
silencing have been better understood thanks to recent advances in biomedical
research.