Methods in molecular biology, Год журнала: 2025, Номер unknown
Опубликована: Янв. 1, 2025
Язык: Английский
Frontiers in Immunology, Год журнала: 2025, Номер 16
Опубликована: Март 17, 2025
Osteoarthritis (OA) is the most common degenerative joint disease worldwide, characterized by synovial inflammation, cartilage loss, and reactive hyperplasia of subchondral bone, affecting quality life hundreds millions people. However, molecular mechanisms underlying occurrence progression OA remain unclear, there no therapy can substantially interrupt or reverse destructive process OA. More insight into pathogenesis may result in innovative therapeutics. The microenvironment plays a pivotal role development OA, which encompasses chondrocytes, adipocytes, fibroblasts, endothelial cells, immune cells. Extracellular vesicles (EVs) have emerged as novel form intercellular communication, mediating transfer range bioactive molecules to create specific microenvironment. Recent studies reported that cargos EVs play crucial including noncoding RNAs (ncRNAs), proteins, lipids. This review systematically analyzes summarizes biological characteristics functionalities derived from diverse cellular sources, especially how mediate communication between different cells microenvironment, with view providing new insights
Язык: Английский
Процитировано
0
Biogerontology, Год журнала: 2025, Номер 26(2)
Опубликована: Фев. 5, 2025
Abstract Neuroinflammation is closely linked to aging, which damages the structure and function of brain. It caused by intricate interactions immune cells in aged brain, such as dysregulated glial dysfunctional astrocytes. Aging-associated chronic low inflammation, referred neuroinflammaging, shows an upregulated proinflammatory response. Autophagy senescence play crucial roles moderators aging neuroinflammatory responses. The neuroimmune system, dystrophic cells, release factors alter blood-brain barrier, causing a landscape. Chronic inflammation combined with deteriorating neurons exacerbate neurological disorders decline cognitive function. This review highlights neuroinflammaging mechanism associated interplay central nervous system cellular senescence, autophagy regulation brain's under conditions. Moreover, microglia peripheral process brain have also been discussed. Determining treatment targets comprehending mechanisms that influence necessary decrease neuroinflammation.
Язык: Английский
Процитировано
0
Journal of Inflammation Research, Год журнала: 2025, Номер Volume 18, С. 1951 - 1967
Опубликована: Фев. 1, 2025
Abstract: Osteoarthritis (OA) is a common degenerative joint disease characterized by the progressive degradation of articular cartilage, synovial inflammation, and subchondral bone remodeling. This review explores interplay between aging, PANoptosis, inflammation in OA progression. Age-related cellular immune dysfunctions, including senescence, senescence-associated secretory phenotypes (SASPs), immunosenescence, significantly contribute to degeneration. In OA, dysregulated apoptosis, necroptosis, pyroptosis, particularly chondrocytes, exacerbate cartilage damage. Apoptosis, mediated JNK pathway, reduces chondrocyte density, while necroptosis involving RIPK-1/RIPK-3 NLRP3 inflammasome, respectively, amplify destruction. Inflammatory cytokines damage-associated molecular patterns (DAMPs) further enhance these PANoptotic pathways. Current therapeutic strategies primarily focus on anti-inflammatory agents such as non-steroidal drugs (NSAIDs) corticosteroids, with growing interest anti-senescence targeting senescence SASP. Additionally, exploring PANoptosis mechanisms offers potential for innovative treatments. Keywords: osteoarthritis,
Язык: Английский
Процитировано
0
International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(4), С. 1567 - 1567
Опубликована: Фев. 13, 2025
Chronic kidney disease (CKD) is a significant public health concern. Osteoarthritis (OA), common form of arthritis, has been shown to have dramatically increased prevalence, particularly among individuals aged 40-50 and older, in the presence CKD. Furthermore, CKD may exacerbate progression impact OA. A survey study revealed that 53.9% patients undergoing long-term hemodialysis were diagnosed with These findings underscore potential association between Uremic toxins, such as indoxyl sulfate, p-cresyl transforming growth factor-β, advanced glycation end-products, are regarded risk factors various CKD-related conditions, affecting bone joint metabolism. However, whether these serve bridging mechanism OA comorbidities, well their detailed roles this context, remains unclear. Addressing identifying effective treatment prevention strategies an urgent challenge warrants immediate attention. This review focuses on describing discussing molecular pathological mechanisms underlying CKD-associated possible therapeutic strategies.
Язык: Английский
Процитировано
0
International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(6), С. 2391 - 2391
Опубликована: Март 7, 2025
Perimenopausal women have fluctuating estrogen levels, which often trigger a range of symptoms perimenopausal syndromes as levels decrease. Changes in are closely related to pain knee osteoarthritis (KOA), has long been research area great interest women. In recent years, it found that an important role KOA pain, namely, can affect through the regulation inflammatory responses, inhibition cellular senescence and apoptosis, modulation neurotransmitters, may provide new ideas for treatment. This study aims describe mechanism level on perimenopause non-pharmacological measures, such physical therapy, factor traditional Chinese medicine, diet, reference treatment with KOA.
Язык: Английский
Процитировано
0
Nature Reviews Rheumatology, Год журнала: 2025, Номер unknown
Опубликована: Март 13, 2025
Язык: Английский
Процитировано
0
Journal of Ethnopharmacology, Год журнала: 2025, Номер unknown, С. 119645 - 119645
Опубликована: Март 1, 2025
Язык: Английский
Процитировано
0
Methods in molecular biology, Год журнала: 2025, Номер unknown
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
0