Advances in Aging and Skeletal Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 939

Special Issue Editors


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Guest Editor
Physiology and Cell Biology, University of Arkansas for Medical Sciences, Little Rock, AR, USA
Interests: bone; senescence; aging; nutrition; cancer

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Guest Editor
Department of Orthopaedic Surgery, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo 060-8638, Japan
Interests: bone; cartilage; osteoimmunology; inflammation; immune cells
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Special Issue Information

Dear Colleagues,

As the global population continues to age, skeletal diseases such as osteoporosis and bone metastatic cancers are becoming increasingly prevalent, imposing a significant socioeconomic burden worldwide. Aging is driven by fundamental mechanisms, including telomere shortening, genomic instability, loss of proteostasis, mitochondrial dysfunction, deregulated nutrient sensing, stem cell exhaustion, altered intercellular communication, and cellular senescence, that contribute to the development and progression of these skeletal disorders. Recent studies, predominantly in animal models, have demonstrated that manipulating these aging mechanisms can extend one’s healthspan, i.e., the period of life free from chronic diseases. Given that these hallmarks of aging are interconnected, targeting one may simultaneously prevent or delay multiple comorbidities, offering a paradigm shift from the current approach of treating individual diseases.

This Special Issue will showcase cutting-edge research on skeletal disorders’ pathophysiological mechanisms, predictive biomarkers, and preclinical therapeutic strategies, with a particular focus on osteoporosis and bone metastatic cancers. We invite authors to contribute original research articles and comprehensive reviews that advance our understanding in these areas.

The topics of interest include but are not limited to the following:

  • Pathophysiological studies related to skeletal diseases;
  • Molecular, biochemical, and biomechanical mechanisms involved in skeletal disorders’ etiology and progression;
  • Identification and validation of biomarkers useful for early diagnosis and/or predictive of prognosis;
  • Preclinical research on potential drugs and cell-based therapies for the treatment of skeletal disorders, particularly osteoporosis and bone metastatic cancers.

Dr. Japneet Kaur
Dr. Mohamad Alaa Terkawi
Guest Editors

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Keywords

  • aging
  • skeletal disorders
  • osteoporosis
  • bone metastatic cancers
  • cellular senescence

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Published Papers (1 paper)

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Research

11 pages, 2190 KiB  
Article
Therapeutic Potential of Targeting Ferroptosis in Periprosthetic Osteolysis Induced by Ultra-High-Molecular-Weight Polyethylene Wear Debris
by Takuya Ogawa, Shunichi Yokota, Liyile Chen, Yuki Ogawa, Yoshio Nishida, Taiki Tokuhiro, Hend Alhasan, Tomoyo Yutani, Tomohiro Shimizu, Daisuke Takahashi, Takuji Miyazaki, Tsutomu Endo, Ken Kadoya, Mohamad Alaa Terkawi and Norimasa Iwasaki
Biomedicines 2025, 13(1), 170; https://doi.org/10.3390/biomedicines13010170 - 13 Jan 2025
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Abstract
Background/Objectives: Periprosthetic osteolysis is the primary cause of arthroplasty failure in the majority of patients. Mechanistically, wear debris released from the articulating surfaces of a prosthesis initiates local inflammation and several modes of regulated cell death programs, such as ferroptosis, which represents a [...] Read more.
Background/Objectives: Periprosthetic osteolysis is the primary cause of arthroplasty failure in the majority of patients. Mechanistically, wear debris released from the articulating surfaces of a prosthesis initiates local inflammation and several modes of regulated cell death programs, such as ferroptosis, which represents a promising therapeutic target in various chronic inflammatory diseases. Thus, the current study aimed at exploring the therapeutic potential of targeting ferroptosis in a polyethylene-wear-debris-induced osteolysis model. Methods: Inverted cell culture model was used for stimulating the cells with wear debris in vitro, and calvarial osteolysis model was used for evaluating the therapeutic effects of inhibitors in vivo. Results: The immunostaining of periprosthetic bone tissues demonstrated a number of osteocytes expressing ferroptosis markers. Likewise, the expressions of ferroptosis markers were confirmed in polyethylene-wear-debris-stimulated osteocyte-like cells and primary osteoblasts in a direct stimulation model but not in an indirect stimulation model. Furthermore, polyethylene wear debris was implanted onto calvarial bone and mice were treated with the ferroptosis inhibitors DFO and Fer-1. These treatments alleviated the inflammatory and pathological bone resorption induced by the wear debris implantation. Conclusions: Our data broaden the knowledge of the pathogenesis of periprosthetic osteolysis and highlight ferroptosis as a promising therapeutic target. Full article
(This article belongs to the Special Issue Advances in Aging and Skeletal Diseases)
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