Clock gene Bmal1 influences the cell cycle of chondrocytes in osteoarthritis DOI
Chunsheng Yang, Mi Chen,

Zulifeiya Aletengbieke

и другие.

Research Square (Research Square), Год журнала: 2024, Номер unknown

Опубликована: Сен. 26, 2024

Abstract Osteoarthritis (OA) is a degenerative disease caused by multiple factors. This study used in vitro and animal models to investigate the connection between biological clock cell cycle osteoarthritic cartilage. The results indicate that transcription levels of circadian gene Bmal1 exhibit negative correlation with Mmp13 positive Wee1. Thus, increased expression Wee1 may be potential protective factor osteoarthritis, while high Per1, Cdk1, Ccnb1, risk factor. By controlling contributing pathophysiology OA, impact apoptosis chondrocytes.

Язык: Английский

Aged bone marrow macrophages drive systemic aging and age-related dysfunction via extracellular vesicle-mediated induction of paracrine senescence DOI Creative Commons
Jing Hou, Kaixuan Chen,

Chen He

и другие.

Nature Aging, Год журнала: 2024, Номер 4(11), С. 1562 - 1581

Опубликована: Сен. 12, 2024

The accumulation and systemic propagation of senescent cells contributes to physiological aging age-related pathology. However, which cell types are most susceptible the aged milieu could be responsible for senescence has remained unclear. Here we found that physiologically bone marrow monocytes/macrophages (BMMs) propagate multiple tissues, through extracellular vesicles (EVs), drive age-associated dysfunction in mice. We identified peroxisome proliferator-activated receptor α (PPARα) as a target microRNAs within BMM-EVs regulates downstream effects on dysfunction. Demonstrating therapeutic potential, report treatment with PPARα agonist fenofibrate effectively restores tissue homeostasis Suggesting conservation humans, cohort study 7,986 participants, use is associated reduced risk chronic disease higher life expectancy. Together, our findings establish BMMs can distant tissues cause dysfunction, they provide supportive evidence extend healthy lifespan.

Язык: Английский

Процитировано

22
Epigenetic regulations of cellular senescence in osteoporosis DOI
Shaochuan Huo,

Xinzheng Tang,

Weijian Chen

и другие.

Ageing Research Reviews, Год журнала: 2024, Номер 99, С. 102235 - 102235

Опубликована: Фев. 16, 2024

Язык: Английский

Процитировано

19
Cellular senescence in the tumor with a bone niche microenvironment: friend or foe? DOI Creative Commons

Sajad Alavimanesh,

Negar Nayerain Jazi,

Maedeh Choubani

и другие.

Clinical and Experimental Medicine, Год журнала: 2025, Номер 25(1)

Опубликована: Янв. 23, 2025

Cellular senescence is understood to be a biological process that defined as irreversible growth arrest and was originally recognized tumor-suppressive mechanism prevents further propagation of damaged cells. More recently, cellular has been shown have dual role in prevention tumor promotion. Senescent cells carry senescence-associated secretory phenotype (SASP), which altered by factors including pro-inflammatory cytokines, chemokines, other proteases, leading the alteration tissue microenvironment. Though would eventually halt cancerous potential cells, SASP contributes environment promoting inflammation, matrix remodeling, cell invasion. The paradox prevention/promotion particularly relevant bone niche microenvironment, where longer-lasting, chronic inflammation promotes formation. Insights into mechanistic understanding provide basis for targeted therapies, such senolytics, aim eliminate senescent or inhibitors, tumor-promoting effects senescence. These therapeutic interventions offer significant clinical implications treating cancer healthy aging.

Язык: Английский

Процитировано

3
Age-related secretion of grancalcin by macrophages induces skeletal stem/progenitor cell senescence during fracture healing DOI Creative Commons

Nan-Yu Zou,

Ran Liu, Mei Huang

и другие.

Bone Research, Год журнала: 2024, Номер 12(1)

Опубликована: Янв. 25, 2024

Abstract Skeletal stem/progenitor cell (SSPC) senescence is a major cause of decreased bone regenerative potential with aging, but the causes SSPC remain unclear. In this study, we revealed that macrophages in calluses secrete prosenescent factors, including grancalcin (GCA), during which triggers and impairs fracture healing. Local injection human rGCA young mice induced delayed repair. Genetic deletion Gca monocytes/macrophages was sufficient to rejuvenate repair aged alleviate senescence. Mechanistically, GCA binds plexin-B2 receptor activates Arg2-mediated mitochondrial dysfunction, resulting cellular Depletion Plxnb2 SSPCs impaired Administration GCA-neutralizing antibody enhanced healing mice. Thus, our study senescent within trigger secondary senescence, neutralization represents promising therapy for nonunion or union elderly individuals.

Язык: Английский

Процитировано

13
Proteostasis disruption and senescence in Alzheimer’s disease pathways to neurodegeneration DOI
Riya Thapa, Asif Ahmad Bhat, Moyad Shahwan

и другие.

Brain Research, Год журнала: 2024, Номер 1845, С. 149202 - 149202

Опубликована: Авг. 30, 2024

Язык: Английский

Процитировано

10
Cellular Senescence and Inflammaging in the Bone: Pathways, Genetics, Anti-Aging Strategies and Interventions DOI Open Access
Merin Lawrence, Abhishek Goyal, Shelly Pathak

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(13), С. 7411 - 7411

Опубликована: Июль 5, 2024

Advancing age is associated with several age-related diseases (ARDs), musculoskeletal conditions impacting millions of elderly people worldwide. With orthopedic contributing towards considerable number patients, a deeper understanding bone aging the need hour. One underlying factors cellular senescence and its secretory phenotype (SASP). SASP comprises pro-inflammatory markers, cytokines chemokines that arrest cell growth development. The accumulation over years leads to chronic low-grade inflammation advancing age, also known as inflammaging. pathways molecular mechanisms focused on inflammaging are currently limited but increasingly being explored. Most genes, involved in coincide those cancer other ARDs like osteoarthritis (OA). Thus, exploring these using techniques sequencing, identifying combatting them most suitable approach crucial for healthy early detection ARDs. Several approaches can be used aid regeneration reduce bone. These may pharmacological, non-pharmacological lifestyle interventions. increasing evidence intricate relationship between aging, senescence, ARDs, anti-aging strategies marrow (BM).

Язык: Английский

Процитировано

7
Unveiling the ageing-related genes in diagnosing osteoarthritis with metabolic syndrome by integrated bioinformatics analysis and machine learning DOI Creative Commons
Jian Huang, Lu Wang,

Jiangfei Zhou

и другие.

Artificial Cells Nanomedicine and Biotechnology, Год журнала: 2025, Номер 53(1), С. 57 - 68

Опубликована: Март 1, 2025

Ageing significantly contributes to osteoarthritis (OA) and metabolic syndrome (MetS) pathogenesis, yet the underlying mechanisms remain unknown. This study aimed identify ageing-related biomarkers in OA patients with MetS. MetS datasets genes (ARGs) were retrieved from public databases. The limma package was used differentially expressed (DEGs), weighted gene coexpression network analysis (WGCNA) screened modules, machine learning algorithms, such as random forest (RF), support vector (SVM), generalised linear model (GLM), extreme gradient boosting (XGB), employed. nomogram receiver operating characteristic (ROC) curve assess diagnostic value, CIBERSORT analysed immune cell infiltration. We identified 20 intersecting among DEGs of OA, key module MetS, ARGs. By comparing accuracy four models for disease prediction, SVM model, which includes CEBPB, PTEN, ARPC1B, PIK3R1, CDC42, selected. These hub ARGs not only demonstrated strong values based on data but also exhibited a significant correlation Building these findings, we have five that are associated infiltration constructed at early diagnosing

Язык: Английский

Процитировано

1
Targeting miR-29 mitigates skeletal senescence and bolsters therapeutic potential of mesenchymal stromal cells DOI
Zhen Ding, Guixing Ma, Bo Zhou

и другие.

Cell Reports Medicine, Год журнала: 2024, Номер 5(8), С. 101665 - 101665

Опубликована: Авг. 1, 2024

Язык: Английский

Процитировано

5
10-hydroxy-2-decenoic acid prevents osteoarthritis by targeting aspartyl β hydroxylase and inhibiting chondrocyte senescence in male mice preclinically DOI Creative Commons

Nana Geng,

Mengtian Fan,

Biao Kuang

и другие.

Nature Communications, Год журнала: 2024, Номер 15(1)

Опубликована: Сен. 4, 2024

Язык: Английский

Процитировано

5
Cellular Senescence: The Driving Force of Musculoskeletal Diseases DOI Creative Commons

Angela Falvino,

Beatrice Gasperini, Ida Cariati

и другие.

Biomedicines, Год журнала: 2024, Номер 12(9), С. 1948 - 1948

Опубликована: Авг. 26, 2024

The aging of the world population is closely associated with an increased prevalence musculoskeletal disorders, such as osteoporosis, sarcopenia, and osteoarthritis, due to common genetic, endocrine, mechanical risk factors. These conditions are characterized by degeneration bone, muscle, cartilage tissue, resulting in fractures reduced mobility. Importantly, a crucial role pathophysiology these diseases has been proposed for cellular senescence, state irreversible cell cycle arrest induced factors DNA damage, telomere shortening, mitochondrial dysfunction. In addition, senescent cells secrete pro-inflammatory molecules, called senescence-associated secretory phenotype (SASP), which can alter tissue homeostasis promote disease progression. Undoubtedly, targeting their profiles could development integrated strategies, including regular exercise balanced diet or use senolytics senomorphs, improve quality life population. Therefore, our review aimed highlight senescence age-related diseases, summarizing main underlying mechanisms potential anti-senescence strategies treatment osteoarthritis.

Язык: Английский

Процитировано

4