Ferroptosis in osteogenic differentiation: a narrative review of bone regeneration metabolism DOI
Lei Huang, Jiayi Wang, Jin Xu

et al.

Regenerative medicine reports ., Journal Year: 2025, Volume and Issue: unknown

Published: May 12, 2025

Bone healing is a complex multifactor and diverse physiological process. In terms of osteogenic differentiation, different types regulated cell death, such as ferroptosis, play key roles in the bone microenvironment. Ferroptosis new type death discovered 2012. It characterized by lipid peroxidation iron-dependent accumulation, which are closely related to various clinical challenges. recent years, an increasing number studies have indicated strong potential relationship between ferroptosis orthopedic diseases, including osteoporosis, osteopenia osteoarthritis. Hence, in-depth investigation metabolism highly important for treatment diseases. Moreover, also accompanied morphological changes mitochondria, increased membrane density shrunken been detected osteoblasts, marrow stem mesenchymal cells osteoclasts. The inhibition can reduce mitochondrial damage, alleviate oxidative stress promote regeneration. This article reviews mechanism from aspects iron overload regulation ferroptosis-related pathways, well their effects on Increasing evidence has shown that defect regeneration processes abnormal metabolism. Inhibiting BMSCs or OBs effectively improve rate progression. We discuss detailed summarize current research disease treatment.

Language: Английский

Asperosaponin VI suppresses ferroptosis in chondrocytes and ameliorates osteoarthritis by modulating the Nrf2/GPX4/HO-1 signaling pathway DOI Creative Commons
Zhimeng Zhang,

Daotong Yuan,

Ximin Jin

et al.

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16

Published: Feb. 28, 2025

Background Asperosaponin VI (AVI) is a naturally occurring monosaccharide derived from Dipsacus asperoides renowned for its anti-inflammatory and bone-protective properties. Objective To elucidate the specific mechanism through which AVI affects chondrocytes in osteoarthritis (OA). Methods For vitro experiments, primary were to molecular mechanisms underlying action of AVI.For vivo rat OA models established using modified Hulth method. The severity knee was evaluated 8 weeks post-surgery. Micro-CT imaging, hematoxylin-eosin staining, Safranin O-fast green staining used assess degeneration joints. Immunohistochemistry techniques conducted measure levels collagen II, MMP13, Nrf2, GPX4, ACSL4, HO-1 within cartilage tissues. ELISA assays performed those TNF-α, IL -6, PGE2 serum samples. Results alleviated chondrocyte apoptosis extracellular matrix degradation induced by IL-1β. It attenuated IL-6, while reducing Fe 2+ malondialdehyde (MDA). upregulated expression HO-1, GPX4 downregulating that ACSL4. Mechanistic studies revealed ML385-induced inhibition Nrf2 signaling pathway reversed increase ACSL4 increased MDA levels; treatment with erastin, ferroptosis inducer, produced comparable results. In experiments demonstrated improved bone volume/tissue volume trabecular separation values rats; Osteoarthritis Research Society International score; expression; downregulated MMP13 expression, decreased PGE2. Conclusion Our findings suggest promising therapeutic agent OA. exerted protective effect regulating Nrf2/GPX4/HO-1 axis inhibit cell improve osteoarthritis.

Language: Английский

Citations

0
Positive regulation Asperosaponin VI accumulation by DaERF9 through JA signaling in Dipsacus asper DOI Creative Commons

Huanhuan Yang,

Jiao Xu,

Chunyun Xu

et al.

BMC Plant Biology, Journal Year: 2025, Volume and Issue: 25(1)

Published: May 9, 2025

Language: Английский

Citations

0
Ferroptosis in osteogenic differentiation: a narrative review of bone regeneration metabolism DOI
Lei Huang, Jiayi Wang, Jin Xu

et al.

Regenerative medicine reports ., Journal Year: 2025, Volume and Issue: unknown

Published: May 12, 2025

Bone healing is a complex multifactor and diverse physiological process. In terms of osteogenic differentiation, different types regulated cell death, such as ferroptosis, play key roles in the bone microenvironment. Ferroptosis new type death discovered 2012. It characterized by lipid peroxidation iron-dependent accumulation, which are closely related to various clinical challenges. recent years, an increasing number studies have indicated strong potential relationship between ferroptosis orthopedic diseases, including osteoporosis, osteopenia osteoarthritis. Hence, in-depth investigation metabolism highly important for treatment diseases. Moreover, also accompanied morphological changes mitochondria, increased membrane density shrunken been detected osteoblasts, marrow stem mesenchymal cells osteoclasts. The inhibition can reduce mitochondrial damage, alleviate oxidative stress promote regeneration. This article reviews mechanism from aspects iron overload regulation ferroptosis-related pathways, well their effects on Increasing evidence has shown that defect regeneration processes abnormal metabolism. Inhibiting BMSCs or OBs effectively improve rate progression. We discuss detailed summarize current research disease treatment.

Language: Английский

Citations

0