{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T13:54:12Z","timestamp":1789480452531,"version":"build-2803163510"},"reference-count":53,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2026,1,26]],"date-time":"2026-01-26T00:00:00Z","timestamp":1769385600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Am J Sports Med"],"published-print":{"date-parts":[[2026,3]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Knee osteoarthritis (KOA) is a common degenerative disease characterized by cartilage degradation and damage. Chondrocyte senescence plays a key role in disease progression, as the accumulation of senescent cells disrupts cellular function and exacerbates cartilage damage. Platelet-rich plasma (PRP), rich in growth factors, promotes tissue repair and regeneration. It remains unclear whether platelet-rich plasma modulates cellular senescence to regulate the progression of knee osteoarthritis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Purpose:<\/jats:title>\n                    <jats:p>To evaluate the effects of PRP on chondrocyte senescence in KOA and investigate its potential underlying mechanisms.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Study Design:<\/jats:title>\n                    <jats:p>Controlled laboratory study.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Chondrocyte cell cycle, senescence markers, senescence-associated secretory phenotype secretion, and extracellular matrix integrity were evaluated by Western blot, real-time quantitative polymerase chain reaction, flow cytometry, immunofluorescence, and \u03b2-galactosidase staining. Mitochondrial function and antioxidative properties were assessed by measuring mitochondrial membrane potential and reactive oxygen species levels. Additionally, a rat KOA model was established by anterior cruciate ligament transection, followed by weekly intra-articular injections of PRP or phosphate-buffered saline for 4 weeks. Knee joint samples were collected at 8 and 12 weeks after surgery for gross morphology, imaging, and histological analysis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>In vitro experiments revealed that PRP inhibited chondrocyte senescence and extracellular matrix degeneration, as evidenced by increased expression of collagen type 2 alpha 1 (COL2A1) and aggrecan (ACAN), and decreased expression of matrix metalloproteinase 13 (MMP13), a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5), cyclin-dependent kinase inhibitor 2A (P16), cyclin-dependent kinase inhibitor 1A (P21), and tumor protein p53 (P53). Additionally, messenger ribonucleic acid (mRNA) expression of interleukin-1\u03b2 (Il1b), interleukin-6 (Il6), and tumor necrosis factor (TNF), as well as \u03b2-galactosidase positivity, was suppressed. Furthermore, PRP was found to modulate cell cycle arrest, improve mitochondrial function, and enhance antioxidative properties. In vivo experiments demonstrated that intra-articular PRP injection repaired damaged articular cartilage, improved trabecular bone parameters, and upregulated the expression of COL2A1 and ACAN, while suppressing the expression of senescence-related proteins P16, P21, and P53 in the cartilage of the KOA model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>Our results demonstrated that PRP may slow osteoarthritis progression by inhibiting chondrocyte senescence.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Clinical Relevance:<\/jats:title>\n                    <jats:p>Chondrocyte senescence plays a critical role in the pathogenesis of osteoarthritis. This study provides new theoretical foundations and experimental support for the clinical application of PRP in the treatment of osteoarthritis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/03635465251408090","type":"journal-article","created":{"date-parts":[[2026,1,27]],"date-time":"2026-01-27T06:49:46Z","timestamp":1769496586000},"page":"831-847","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":3,"title":["Effects of Platelet-Rich Plasma on Chondrocyte Senescence and Knee Osteoarthritis Progression"],"prefix":"10.1177","volume":"54","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-6832-6795","authenticated-orcid":false,"given":"Jiang-Yin","family":"Zhang","sequence":"first","affiliation":[{"name":"Rehabilitation Medicine Center and Institute of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, P.R. 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