Single-Cell Profiling Reveals a Protective WNT5A-ATF3-FOSB Signaling Axis in Hair Follicle Stem Cells During Androgenetic Alopecia.

One common long-term degenerative joint condition is osteoarthritis (OA). OA is predicted to impact 355 million people globally by 2024, and its incidence will continue to climb every year. Osteoarthritis is more common in women, obese individuals, and those with a history of joint damage (). Degenerative changes in articular cartilage, along with subchondral bone sclerosis, osteophyte formation, subchondral cystic alterations, thickening of the joint capsule, and injury to muscles and ligaments, are the pathological features of osteoarthritis. These changes eventually jeopardize the entire joint structure by accelerating the deterioration of articular cartilage. (). While osteoarthritis is still characterized by cartilage degradation, subchondral bone has become more important in recent years. The subchondral bone plate and the underlying trabecular bone make up subchondral bone, which together give the cartilage on top mechanical support (). The subchondral bone plate connects to the bone trabeculae below, which are abundant in blood vessels, nerves, and other kinds of bone cells, and supports the articular cartilage upward. According to new research, osteoclast activation may change the kinetics of bone remodeling, which is regulated by local oxygen concentration and H-type blood vessels. This could lead to cartilage malfunction (). The bidirectional interaction between subchondral bone and cartilage is now recognized as a key driver of OA progression and associated pain. The recently emerging subject of immunometabolism is intimately linked to this complex interaction mechanism (; ). This fundamental idea is determined by how the immune system and cell metabolism interact, as suggested by , . The metabolic reprogramming of immune cells, such as oxidative phosphorylation and anaerobic glycolysis, is the basis of immunometabolism and serves to meet the energy and biosynthetic material requirements of immune cells. Thus, these pathways directly control the inflammatory response in chronic illnesses and also encourage metabolic reprogramming as fundamental upstream regulators.