Mitochondria in skeletal system-related diseases DOI Open Access

Liang Pei,

Zizhen Yao, Liang Dong

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 181, P. 117505 - 117505

Published: Nov. 4, 2024

Language: Английский

FSH exacerbates bone loss by promoting osteoclast energy metabolism through the CREB-MDH2-NAD+ axis DOI

Jingqiu Chen,

Yilin Liao, Yue Sheng

et al.

Metabolism, Journal Year: 2025, Volume and Issue: unknown, P. 156147 - 156147

Published: Jan. 1, 2025

Language: Английский

Citations

2

Dectin-2 depletion alleviates osteoclast-induced bone loss in periodontitis via Syk/NOX2/ROS signaling DOI

W. Ye,

Yi-Lin Liao,

Xiaoyu Liu

et al.

Free Radical Biology and Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

Citations

0

Mitophagy and Its Significance in Periodontal Disease DOI Open Access

Guliqihere Abulaiti,

Xu Qin, Lili Chen

et al.

Oral Diseases, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 10, 2025

Periodontal disease is a common chronic inflammatory condition affecting the tissues that support teeth, leading to their destruction. Mitophagy, specialized form of autophagy responsible for degrading damaged mitochondria, plays crucial role in maintaining cellular homeostasis. However, its periodontal progression remains poorly understood. This review aims summarize recent research on mitophagy's pathogenesis. A comprehensive literature mitophagy was conducted using PubMed, Scopus, and Web Science databases, employing keywords related such as "periodontal," "periodontitis," "gingiva," "gingivitis." 18 original studies revealed by regulating key pathophysiological mechanisms. Specifically, modulates inflammation influencing pro-inflammatory cytokines mitochondrial reactive oxygen species. Additionally, it essential alveolar bone remodeling, impacting both resorption regeneration. Mitophagy also regulates cell apoptosis within tissues, helping preserve function tissue integrity during progression. pathogenesis modulating inflammation, death tissues. Further needed explore therapeutic potential treatment improve targeted interventions.

Language: Английский

Citations

0

From death to birth: how osteocyte death promotes osteoclast formation DOI Creative Commons
Weijie Zhao, Jiale Qian, Ji Li

et al.

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

Published: March 17, 2025

Bone remodeling is a dynamic and continuous process involving three components: bone formation mediated by osteoblasts, resorption osteoclasts, formation-resorption balancing regulated osteocytes. Excessive osteocyte death found in various diseases, such as postmenopausal osteoporosis (PMOP), osteoclasts are increased activated at sites. Currently, apart from apoptosis necrosis previously established, more forms of cell reported, including necroptosis, ferroptosis pyroptosis. These play important role the development inflammatory diseases diseases. Increasing studies have revealed that promote osteoclast via different mechanism, actively secreting pro-inflammatory pro-osteoclastogenic cytokines, tumor factor alpha (TNF-α) receptor activator nuclear factor-kappa B ligand (RANKL), or passively releasing damage associated molecule patterns (DAMPs), high mobility group box 1 (HMGB1). This review summarizes established potential mechanisms which regulate formation, aiming to provide better understanding disease therapeutic target.

Language: Английский

Citations

0

Research Progress on the Biological Activity of Isobavachin DOI

文渊 张

Journal of Organic Chemistry Research, Journal Year: 2025, Volume and Issue: 13(01), P. 70 - 76

Published: Jan. 1, 2025

Language: Английский

Citations

0

Causal Relationship between Mitochondrial Biological Function and Periodontitis: Evidence from a Mendelian Randomization Study DOI Open Access
Huan Zhou,

Yan-Xin Qi,

Ruoyan Cao

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(14), P. 7955 - 7955

Published: July 21, 2024

A growing number of studies indicate that mitochondrial dysfunction serves as a pathological mechanism for periodontitis. Therefore, this two-sample Mendelian randomization (MR) study was carried out to explore the causal associations between biological function and periodontitis, because specific nature relationship remains inconclusive in existing MR studies. Inverse variance weighting, randomization-Egger, weighted mode, simple median analyses were performed assess relationships exposure factors The results present revealed association periodontitis medium-chain acyl-CoA dehydrogenase (MCAD), malonyl-CoA decarboxylase (MLYCD), glutaredoxin 2 (Grx2), oligoribonuclease (ORN), pyruvate carboxylase (PC). Notably, MCAD MLYCD are causally linked serve protective factors. However, Grx2, ORN, PC risk Our established such insights may provide promising approach treating via regulation.

Language: Английский

Citations

1

Mitochondria in skeletal system-related diseases DOI Open Access

Liang Pei,

Zizhen Yao, Liang Dong

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 181, P. 117505 - 117505

Published: Nov. 4, 2024

Language: Английский

Citations

1