Abstract
Osteoporosis is a prevalent bone disorder characterized by bone mass reduction and deterioration of bone microarchitecture leading to bone fragility and fracture risk. In recent decades, knowledge regarding the etiological mechanisms emphasizes that inflammation, oxidative stress and senescence of bone cells contribute to the development of osteoporosis. Studies have demonstrated that heme oxygenase 1 (HO-1), an inducible enzyme catalyzing heme degradation, exhibits anti-inflammatory, anti-oxidative stress and anti-apoptosis properties. Emerging evidence has revealed that HO-1 is critical in the maintenance of bone homeostasis, making HO-1 a potential target for osteoporosis treatment. In this Review, we aim to provide an introduction to current knowledge of HO-1 biology and its regulation, focusing specifically on its roles in bone homeostasis and osteoporosis. We also examine the potential of HO-1-based pharmacological therapeutics for osteoporosis and issues faced during clinical translation.
Highlights
Osteoporosis, the most common bone disorder, is characterized by decreased bone mineral density (BMD), deterioration of bone microarchitecture and poor mechanical properties, resulting in increased vulnerability to fractures (NIH Consensus Development Panel on Osteoporosis Prevention and Therapy, 2000; van den Bergh et al, 2012; Vestergaard et al, 2007)
It has been reported that human peripheral-blood monocytes (PBMCs) from osteoporosis patients have 29–67% higher secretion of IL-1β, IL-6, and TNF-α in whole blood culture compared with healthy control subjects (Pacifici et al, 1987)
The results showed that resveratrol (75 mg, twice daily) positively augmented BMD in the lumbar spine and femoral neck together with a 7.24% reduction in CTx (C-telopeptide of type I collagen, a marker of bone resorption)
Summary
Osteoporosis, the most common bone disorder, is characterized by decreased bone mineral density (BMD), deterioration of bone microarchitecture and poor mechanical properties, resulting in increased vulnerability to fractures (NIH Consensus Development Panel on Osteoporosis Prevention and Therapy, 2000; van den Bergh et al, 2012; Vestergaard et al, 2007). Osteoporosis is the result of an imbalance in bone remodeling which is a dynamic process that involves both bone formation and resorption (Langdahl et al, 2016). For this reason, current pharmacological treatments of osteoporosis primarily are antiresorptive (inhibiting the osteoclasts, e.g., estrogen and bisphosphonates), bone forming (stimulating the osteoblasts, e.g., parathyroid hormone) or dual acting (e.g., romosozumab) (Langdahl, 2021). Extensive studies regarding the etiological mechanisms underpinning osteoporosis have emphasized that oxidative stress, inflammation and cellular senescence contribute to the progression of osteoporosis, indicating
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