Tissue & cell最新文献

{"title":"DNMT1-mediated LAMA2 inhibition induces M2 macrophage polarization during prostate cancer progression","authors":"Ruiqian Li ,&nbsp;Chen Hu ,&nbsp;Fengming Ran ,&nbsp;Yu Bai ,&nbsp;Hongyi Wu ,&nbsp;Wenjun Peng ,&nbsp;Yixuan He ,&nbsp;Qilin Wang ,&nbsp;Jun Li","doi":"10.1016/j.tice.2025.103173","DOIUrl":"10.1016/j.tice.2025.103173","url":null,"abstract":"<div><h3>Background</h3><div>Prostate cancer (PCa) presents a significant risk to the health of men, and its metastatic spread greatly affects patient survival rates and quality of life. This research investigated the role of DNA methyltransferase 1 (DNMT1) in the progression of PCa.</div></div><div><h3>Methods</h3><div>By performing bioinformatics analysis and in vivo and in vitro experiments, we investigated the expression levels of DNMT1 and LAMA2 in PCa. Additionally, we evaluated how they influence the proliferation and tumor microenvironment (TME) of PCa cells.</div></div><div><h3>Results</h3><div>DNMT1 was upregulated in PCa, whereas LAMA2 was downregulated. DNMT1 inhibited the expression of LAMA2 by promoting methylation of the LAMA2 promoter, thereby activating the PI3K/AKT signaling pathway, promoting the proliferation of PCa cells, and inducing M2 polarization of macrophages in the TME. Furthermore, DNMT1 promoted the release of the cytokines CCL5, VEGF, MMP9, and PTX3 by PC-3 cells and affected the TME.</div></div><div><h3>Conclusion</h3><div>This research highlights the crucial function of DNMT1 in the progression of PCa, providing new strategies for the treatment of PCa, particularly therapeutic strategies that focus on DNA methylation and tumor-associated macrophages.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103173"},"PeriodicalIF":2.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145226954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in cell therapy for testicular cancer: a comprehensive overview of immunotherapy and stem cell therapy.","authors":"Farhood Khaleghi Mehr, Nikoo Emtiazi, Ehsan Zolfi","doi":"10.1016/j.tice.2025.103169","DOIUrl":"https://doi.org/10.1016/j.tice.2025.103169","url":null,"abstract":"<p><p>Testicular Cancer is the most common type of cancer in teenage and young adult men. Most cases correspond to testicular germ cell tumors (TGCTs). Testicular cancer treatment must be customized to minimize long-term side effects, protect quality of life, and increase cure rates. Developing new ways to treat testicular cancer is crucial if we want to reduce the side effects of current treatments and maximize their effectiveness. Opportunities to investigate the efficacy of immunotherapeutic drugs, particularly immune checkpoint inhibitors (ICIs), in various types of cancers, including germ cell tumors (GCTs), have arisen due to recent advancements. Immunotherapy is a hotspot for research in the fight against metastatic or cisplatin-resistant testicular cancer, a disease that has so far defied conventional medicine. Thus, new avenues for treating TGCT patients have emerged with the introduction of immunotherapy. Cancer-testis antigens (CTAs) are a group of genes that are exclusively expressed in cancer cells and specific germline cells. Much work is being done with CTAs to develop tumor vaccines and T-cell treatments. It has been successful in treating people with germ-cell tumors that have returned or are not responding to treatment with high-dose chemotherapy and autologous stem cell transplants. Stem cell therapy also offers exciting new approaches to treating testicular cancer, including the potential to target cancer cells, enhance fertility, regulate hormone function, and alleviate the side effects of long-term treatment. This study examined the role of immunotherapy, including T cells, NK cells, dendritic cells, and macrophages, in treating testicular cancer. We've also discussed how stem cells and their offspring, such as extracellular vesicles, can be used to treat testicular cancer.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"103169"},"PeriodicalIF":2.5,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145259206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pioglitazone improves tamoxifen-induced renal injury in rat model through modulating oxidative stress, inflammation, and apoptosis signaling","authors":"Gellan Alaa Mohamed Kamel ,&nbsp;Shaimaa Hussein","doi":"10.1016/j.tice.2025.103154","DOIUrl":"10.1016/j.tice.2025.103154","url":null,"abstract":"<div><div>One prevalent chemotherapeutic medication used to treat breast cancer is tamoxifen (TAM), and several off-label uses. However, when used as an antineoplastic drug in clinical settings, it causes harmful cellular effects such as renal damage. The mechanisms underlying TAM-induced kidney injury primarily involve oxidative stress and inflammatory pathways. Pioglitazone (PIO), an agonist of peroxisome proliferator-activated receptor-gamma (PPAR-γ), is a medication primarily indicated for type 2 diabetes mellitus. Beyond its hypoglycemic actions, PIO exhibits potent anti-inflammatory and antioxidant effects, which have been documented in various tissues. Hence, this study investigates the potential protective effects of PIO on TAM-induced renal impairment, revealing their possible protective mechanisms. The rats were orally administered doses of PIO (10 mg/kg) and TAM (45 mg/kg) over ten days. Renal histopathological changes, kidney function, and biochemical examination are conducted. TAM raised serum creatinine and urea levels, leading to histopathological changes, renal oxidative stress, and elevated expression of NF-κB p65 and proinflammatory cytokines. Conversely, PIO treatment exerted a protective effect and attenuated TAM-induced nephrotoxicity. Significantly, malondialdehyde (MDA) and proinflammatory markers were reduced while enhancing renal antioxidant activity. Furthermore, renal Nrf2, HO-1, Bcl-2 expression while lowering NF-κB, KIM-1, Bax and caspase-3 levels. In conclusion, PIO demonstrated significant nephroprotective effects against TAM-induced renal damage by inhibiting apoptosis, reducing inflammation, and counteracting oxidative stress.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103154"},"PeriodicalIF":2.5,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential effects of type I, III, and V collagens on mammary epithelial development in vitro","authors":"Kazuki Ninomiya,&nbsp;Yuki Yasui,&nbsp;Liang Han,&nbsp;Tamaki Uehara,&nbsp;Takanori Nishimura,&nbsp;Ken Kobayashi","doi":"10.1016/j.tice.2025.103165","DOIUrl":"10.1016/j.tice.2025.103165","url":null,"abstract":"<div><div>During pregnancy, mammary epithelial cells (MECs) and myoepithelial cells proliferate and develop ductal networks and alveolar bud structures that extend into the surrounding stroma. In the mammary stroma, type I, III, and V collagens form fibrillar structures and dynamically alter their expression patterns. While type I collagen is known to influence ductal elongation and alveolar bud formation, the specific roles of type III and V collagen in mammary epithelial morphogenesis remain unclear. This study aimed to create three-dimensional (3D) cultures by embedding mammary organoids in Matrigel with type I, III, and V collagen to explore their distinct roles in mammary duct elongation and alveolar bud formation in vitro. We prepared 3D organoid cultures of MECs and myoepithelial cells within type I, III, and V collagen gels to reproduce ductal elongation and alveolar bud formation. Type I collagen promoted ductal elongation and alveolar bud formation in a density-dependent manner. In contrast, type III collagen suppressed these morphogenetic processes compared to type I collagen. Type V collagen induced the formation of narrow ducts and swollen alveolar-like structures. Type III and V collagens reduced cell proliferation and attenuated Akt and ERK signaling relative to type I collagen. Myoepithelial cells were absent from ductal and alveolar regions in type I and V collagen gels but encircled the organoids in type III collagen gels. Scanning electron microscopy revealed distinct fibrillar architectures among the three collagen types. These findings demonstrate that collagens I, III, and V exert distinct regulatory effects on mammary epithelial morphogenesis during pregnancy.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103165"},"PeriodicalIF":2.5,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145207700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Naringenin mitigates 5-fluorouracil-induced nephrotoxicity by decreasing oxidative stress, inflammation and apoptosis","authors":"Fatih Mehmet Gür ,&nbsp;Sedat Bilgiç ,&nbsp;İbrahim Aktaş","doi":"10.1016/j.tice.2025.103170","DOIUrl":"10.1016/j.tice.2025.103170","url":null,"abstract":"<div><div>The toxic effects of 5-fluorouracil (5-FU), a drug widely used in the treatment of neoplasms and primarily excreted through the urine, prompted us to investigate the protective potential of naringenin (NAR) against nephrotoxicity induced by 5-FU. In this study, 28 rats were randomly allocated to four groups: Control, NAR (100 mg/kg/day), 5-FU (150 mg/kg), and NAR + 5-FU (n = 7). After completion of the experimental procedures, blood and kidney tissues were subjected to analysis through biochemical, immunohistochemical, TUNEL, and histopathological methods. The analyses demonstrated significantly higher levels of MDA, BUN, TNF-α, caspase-3, and apoptosis in the 5-FU group compared to the control. Pathological alterations, including inflammatory cell infiltration, interstitial hemorrhage, brush border damage, epithelial desquamation, vacuolar degeneration, and basement membrane thickening, observed in the 5-FU group were largely absent in the NAR +5-FU group. In conclusion, NAR can significantly prevent the nephrotoxic effects of 5-FU due to its antioxidant, anti-inflammatory, and anti-apoptotic properties. The findings support the view that the therapeutic effects of NAR are mediated through the upregulation of Nrf2 and the downregulation of NF-κB.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103170"},"PeriodicalIF":2.5,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145207702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nepetin attenuates sertraline-induced cardiac dysfunction by modulating notch signaling, oxidative stress, and inflammation: Echocardiographic and histological evidence","authors":"Hassan M. Otifi ,&nbsp;Muhammad Faisal Hayat ,&nbsp;Aqsa Bibi ,&nbsp;Hesham M. Hassan ,&nbsp;Ahmed Al-Emam","doi":"10.1016/j.tice.2025.103163","DOIUrl":"10.1016/j.tice.2025.103163","url":null,"abstract":"<div><h3>Background</h3><div>(STL) is an extensively used anti-depressant drug that has been reported to induce organ damage including cardiac impairments. Nepetin (NEP) is a naturally derived flavonoid which exhibits excellent biological as well as pharmacological properties.</div></div><div><h3>Methodology</h3><div>This research investigation explored the cardioprotective ability of NEP to counter STL induced cardiotoxicity in Sprague Dawley rats. Thirty-six male Sprague Dawley rats were categorized into control, STL (20 mg/kg), STL (20 mg/kg) + NEP (10 mg/kg), and NEP (10 mg/kg) alone treated group.</div></div><div><h3>Results</h3><div>NEP intoxication significantly suppressed the expression of Notch 1, JAG1, DDL4, HES1, and HEY2 while escalating the levels of ROS and MDA. Besides, STL administration increased intraventricular septal thickness during IVSd and IVSs, promoted the internal diameter of left ventricular as well as elevated ESV as while reducing PWs and PWd, LVEF, and LVFS in echocardiographic examination. The enzymatic activities of HO-1, SOD, GPx, GSR, GST, CAT, and contents of GSH were reduced while the levels of CPK, ProBNP, troponin-T, CK-MB, LDH, C-reactive protein, BNP, and troponin-I were promoted after STL intoxication. Moreover, the levels of COX-2, IL-6, TNF-α, NF- κB, and IL-1β were elevated after STL exposure. Histopathological analysis showed abnormal cardiac architecture following the administration of STL. Importantly, NEP therapy significantly conferred cardio-protection via regulating redox state, reactivating Notch signaling, suppressing inflammatory responses, and improving histopathological alterations. Moreover, echocardiographic parameters were also found normal after NEP supplementation. These findings highlight the cardioprotective role of NEP in mitigating anti-depressant drugs induced cardiotoxicity.</div></div><div><h3>Conclusion</h3><div>NEP confers cardio-protection against STL-induced cardiotoxicity via regulating oxidative stress, notch signaling, inflammation and cardiac function markers. These findings suggest this compound a promising therapy to mitigate anti-depressant drug-induced cardiac damage.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103163"},"PeriodicalIF":2.5,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145226855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ameliorative effects of hesperidin against iohexol-induced acute kidney injury: Modulating the levels of NF-κB/TNF-α/IL-1β, JAK2/STAT3, and Wnt3a/Dvl-2 signaling pathways.","authors":"Fatih Mutlu, Hüseyin Mutlu, Özge Kandemir, Nurhan Akaras, Hasan Şimşek, Cuneyt Caglayan, Fatih Mehmet Kandemir","doi":"10.1016/j.tice.2025.103166","DOIUrl":"https://doi.org/10.1016/j.tice.2025.103166","url":null,"abstract":"<p><p>Iohexol is a non-ionic contrast agent widely used in diagnostic imaging and angiographic procedures; however, its administration carries the risk of contrast-induced nephropathy. This study was conducted to investigate the ameliorative effects of hesperidin use against iohexol-induced acute kidney injury (AKI) in rats. Male wistar albino rats were randomly assigned into five groups: i) control, ii) hesperidin (100 mg/kg/day orally), iii) iohexol (3 g/kg, i.p), iv) iohexol (3 g/kg) and hesperidin (100 mg/kg) and v) iohexol (3 g/kg) and hesperidin (200 mg/kg). The induction of AKI was performed by dehydration and the administration of contrast media (iohexol) and inhibitors of prostaglandin (indomethacin) and nitric oxide synthesis (L-NAME: N-nitro L-arginine methyl ester). Hesperidin was administered for two weeks before the induction of AKI. Results showed that iohexol induced significant histopathological kidney damage and increased serum urea and creatinine levels. Molecular analyses revealed that iohexol suppressed AQP1 and AQP2 expression, while upregulating KIM-1 and inflammatory markers such as MAPK14, JAK2/STAT3, TRAF6/ACT1/IL-17A, and NFκB/TNF-α/IL-1β at the gene expression level. Furthermore, iohexol decreased the measured activity of antioxidant enzymes (SOD, CAT and GPx) and the GSH content, and significantly increased MDA levels. Additionally, iohexol promoted apoptosis mediated by Caspase-3, Bax, and Bcl-2, and suppressed gene expression of Wnt3a/Dvl-2 and Cyclin D1, which are involved in cell cycle regulation and development. This is the first study to link hesperidin with modulation of Wnt3a/Dvl-2 signaling in iohexol-induced AKI. Hesperidin treatment significantly modulated these parameters, demonstrating a nephroprotective effect. Thus, it was supported that hesperidin could be a potential nephroprotective agent.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"103166"},"PeriodicalIF":2.5,"publicationDate":"2025-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145245438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CAR T-cell therapy in autoimmune diseases: Opportunities and challenges, with implications for RA","authors":"Mohamad mahdi Hojati shargh ,&nbsp;Mahmoud Mahmoudi ,&nbsp;Seyed Amir Asef Agah ,&nbsp;Fatemeh Forouzanfar ,&nbsp;Zahra Javanmardi ,&nbsp;Afsane Fadaee ,&nbsp;Dariush Haghmorad ,&nbsp;Seyed-Alireza Esmaeili","doi":"10.1016/j.tice.2025.103164","DOIUrl":"10.1016/j.tice.2025.103164","url":null,"abstract":"<div><div>Chimeric antigen receptor (CAR) T-cell therapy, initially developed for hematologic malignancies, is now being applied to autoimmune diseases. This review examines CAR T-cell applications in autoimmunity, focusing on rheumatoid arthritis (RA). We analyze CAR T-cell technology development, generational evolution, and manufacturing considerations. Clinical trials in systemic lupus erythematosus (SLE), systemic sclerosis (SSc), and other autoimmune conditions demonstrate that single CAR T-cell infusions induce sustained, drug-free remission through selective pathogenic B-cell depletion and immune tolerance restoration. RA presents distinct challenges: disease heterogeneity, multi-cellular involvement (autoreactive T/B cells, synovial fibroblasts), and absence of universal target antigens. Preclinical approaches include HLA-DR1-targeted CARs for autoreactive CD4 + T cells and anti-FITC CARs for citrullinated peptide-specific B cells, though clinical optimization remains necessary. RA requires higher therapeutic precision than other autoimmune diseases due to established effective conventional treatments. Advances in allogeneic CAR T cells, dual-targeting constructs, and safety mechanisms (suicide switches) may facilitate clinical implementation. This review evaluates CAR T-cell therapy potential in autoimmune disease treatment and RA-specific therapeutic challenges.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103164"},"PeriodicalIF":2.5,"publicationDate":"2025-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Purinergic ion channel-type P2X7 receptor regulates SK3 channel to promote the progression of gastric cancer","authors":"Pin Wan ,&nbsp;Chang-bing Wu","doi":"10.1016/j.tice.2025.103162","DOIUrl":"10.1016/j.tice.2025.103162","url":null,"abstract":"<div><div>The purpose of this study was to investigate the effect of the purinergic ion channel-type P2X7 receptor (P2X7R) on the progression of gastric cancer (GC). Therefore, in this study, <em>in vivo and in vitro</em> experiments were performed to investigate the molecular mechanism of P2X7R on the progression of GC. The results showed that adenosine triphosphate (ATP) and benzoyl ATP (BzATP) activate P2X7R and increased the intracellular calcium concentration of 7901 and 803 cells, and enhanced the migration abilities of GC cells. While P2X7R antagonists (A438079 and AZD9056) decreased the ATP-induced calcium influx, and inhibited the migration abilities of GC cells. This may be related to the stress of actin fibers, which causes the change in cell morphology. Moreover, activation of P2X7R increased the expression of small-conductance Ca^2 + -activated K⁺ channel (SK3) and promoted the migration of GC cells. While A438079 or siRNA transfected cells to knock down the expression of P2X7R and reduced the expression of SK3. The use of SK3 channel inhibitor Apamin inhibited ATP-induced calcium influx and the migration of GC cells. It is interesting that Apamin and A438079 or AZD9056 have a synergistic inhibitory effect. Furthermore, <em>in vivo</em> experiments showed that ATP induced tumor growth, while AZD9056 inhibited ATP-induced tumor growth. Our conclusion is that P2X7R activation promotes the migration and growth of GC cells by opening SK3 channel, and also indicates that P2X7R may become a new potential target for GC treatment.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103162"},"PeriodicalIF":2.5,"publicationDate":"2025-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crosstalk between programmed cell death in chondrocytes-a molecular mechanism of osteoarthritis","authors":"Kun Zhang ,&nbsp;Lianlin Zeng ,&nbsp;Huiqin Min ,&nbsp;Xiaoqian Jiang ,&nbsp;Yangan Li ,&nbsp;Kehui Hu","doi":"10.1016/j.tice.2025.103161","DOIUrl":"10.1016/j.tice.2025.103161","url":null,"abstract":"<div><div>The pathogenesis of osteoarthritis (OA), particularly knee osteoarthritis, is unknown, which is a chronic inflammatory systemic disease. Pathologically, the disease is primarily defined by alterations including cartilage degeneration and joint space decrease, which can result in joint deformity and loss of function. While the drugs currently used to treat OA can be helpful, their adverse effects are so obvious that they need to be further modified. Therefore, a detailed analysis of the mechanisms underlying the initiation and progression of OA is necessary to identify novel treatment targets. Much emphasis has been paid to the significant role that programmed cell death (PCD) plays in OA, particularly in chondrocytes and synoviocytes, where PCD is particularly dysregulated. This paper summarizes the regulatory roles of several types of PCD in OA, including the apoptosis, necroptosis, and autophagy as well as the more recently identified NETosis, pyroptosis, ferroptosis, and cuproptosis. We also discuss the regulatory roles of these processes in chondrocytes, synoviocytes, and other cells. These findings not only provide a vital theoretical basis for enhancing clinical OA treatment practices, but they also point the way toward the development of new target drugs.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103161"},"PeriodicalIF":2.5,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}