Calcified Tissue International, Год журнала: 2023, Номер 113(1), С. 1 - 3
Опубликована: Июль 1, 2023
Язык: Английский
Calcified Tissue International, Год журнала: 2023, Номер 113(1), С. 1 - 3
Опубликована: Июль 1, 2023
Язык: Английский
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
2Ageing Research Reviews, Год журнала: 2024, Номер 99, С. 102235 - 102235
Опубликована: Фев. 16, 2024
Язык: Английский
Процитировано
12Nature 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
11Bone 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
10Brain Research, Год журнала: 2024, Номер 1845, С. 149202 - 149202
Опубликована: Авг. 30, 2024
Язык: Английский
Процитировано
8International 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
6Cell Reports Medicine, Год журнала: 2024, Номер 5(8), С. 101665 - 101665
Опубликована: Авг. 1, 2024
Язык: Английский
Процитировано
4Nature Communications, Год журнала: 2024, Номер 15(1)
Опубликована: Сен. 4, 2024
Язык: Английский
Процитировано
4Опубликована: Фев. 11, 2025
Article Vascular and Metabolic Responses to Elevated Circulating PDGF-BB in Mice: A Multiparametric MRI Study Xiuli Yang 1,†, Jiekang Wang 2,3,†, Yuguo Li 1,4, Mei Wan 2,3,*, Zhiliang Wei 1,4,* 1 Russell H. Morgan Department of Radiology Radiological Science, Johns Hopkins University School Medicine, Baltimore, MD 21205, USA 2 Orthopaedic Surgery, 3 Biomedical Engineering, 4 F. M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, * Correspondence: [email protected] (M.W.); [email protected] (Z.W.) † These authors contributed equally this work. Received: 20 November 2024; Revised: December Accepted: 22 January 2025; Published: 11 February 2025 Abstract: circulating platelet-derived growth factor-BB (PDGF-BB) has been implicated the development various aged-related pathologies is recognized as a potential pro-aging factor. Although numerous studies have explored pathological roles PDGF-BB/PDGFRβ signaling pathway, few investigations dissected its function neurofunctional responses elevated PDGF-BB, primarily because in-vivo measurements are generally required assess neurofunction. To address knowledge gap, we characterized vascular metabolic vivo using multiparametric non-invasive non-contrast techniques conditional Pdgfb transgenic mouse model (PdgfbcTG) at 6 months age. Results indicated that PdgfbcTG mice exhibited decreased cerebral blood flow (p = 0.025), oxygen extraction 0.002), increased rate 0.035), mirroring changes observed human aging. The change was significantly higher (≥200.3%) compared naturally aged mice. This study provides evidence accelerates neurovascular
Язык: Английский
Процитировано
0Progress in Biophysics and Molecular Biology, Год журнала: 2025, Номер unknown
Опубликована: Фев. 1, 2025
Язык: Английский
Процитировано
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