Cellular senescence refers to a process induced by various types of stress that causes irreversible cell cycle arrest and distinct cellular alterations, including profound changes in gene expression, metabolism, and chromatin organization as well as activation/ reinforcement of anti-apoptotic pathways and development of a pro-inflammatory secretome or senescence-associated secretory phenotype (SASP). New findings indicated that senescent cells and their SASP may play a vital role in the development of musculoskeletal system diseases, such as osteoarthritis (OA), osteoporosis (OP), or osteonecrosis of the femoral head (ONFH), et al. The underlying mechanism may be the accumulation of senescent cells or their SASP at sites of pathology or old tissues. And some encouraging results find Seno-therapeutics by targeting senescent cells or inhibiting some specific SASP, such as IL-6, TNF-a, et al, could provide benefits for cartilage regeneration or bone remodeling in preclinical models. While a number of scientific issues need to be uncovered, such as the crosstalk between senescent and their neighborhood healthy cells, the main cell type that becomes senescent in the development and pathology of bone and cartilage, and the link between senescent cells and local or system immune system.
The goal of this research topic is to provide a forum for advancing research on the contribution of cellular senescence to the development and pathology of bone and cartilage, as well as to explore innovative seno-therapeutics in an attempt to provide new treatment options for musculoskeletal disease.
In this research topic, we welcome the submission of Original Research, Review, Mini Review, Clinical Trial, Perspective, and Opinion articles, focusing on but not limited to the following topics:
- The new preclinical or clinical evidence of the role of cellular senescence in OA or OP;
- The interplay between senescence cells and local or system immune cells, such as macrophage, or T cells;
- The internal relationship between aging, immunity, and inflammation;
Cellular senescence refers to a process induced by various types of stress that causes irreversible cell cycle arrest and distinct cellular alterations, including profound changes in gene expression, metabolism, and chromatin organization as well as activation/ reinforcement of anti-apoptotic pathways and development of a pro-inflammatory secretome or senescence-associated secretory phenotype (SASP). New findings indicated that senescent cells and their SASP may play a vital role in the development of musculoskeletal system diseases, such as osteoarthritis (OA), osteoporosis (OP), or osteonecrosis of the femoral head (ONFH), et al. The underlying mechanism may be the accumulation of senescent cells or their SASP at sites of pathology or old tissues. And some encouraging results find Seno-therapeutics by targeting senescent cells or inhibiting some specific SASP, such as IL-6, TNF-a, et al, could provide benefits for cartilage regeneration or bone remodeling in preclinical models. While a number of scientific issues need to be uncovered, such as the crosstalk between senescent and their neighborhood healthy cells, the main cell type that becomes senescent in the development and pathology of bone and cartilage, and the link between senescent cells and local or system immune system.
The goal of this research topic is to provide a forum for advancing research on the contribution of cellular senescence to the development and pathology of bone and cartilage, as well as to explore innovative seno-therapeutics in an attempt to provide new treatment options for musculoskeletal disease.
In this research topic, we welcome the submission of Original Research, Review, Mini Review, Clinical Trial, Perspective, and Opinion articles, focusing on but not limited to the following topics:
- The new preclinical or clinical evidence of the role of cellular senescence in OA or OP;
- The interplay between senescence cells and local or system immune cells, such as macrophage, or T cells;
- The internal relationship between aging, immunity, and inflammation;