Translational research : the journal of laboratory and clinical medicine最新文献

{"title":"Convergent Ferroptosis and Pyroptosis in MASLD-Associated Cardiac Remodeling.","authors":"Huayang Gui, Xingxing Yuan, Yali Zhang","doi":"10.1016/j.trsl.2026.10.007","DOIUrl":"https://doi.org/10.1016/j.trsl.2026.10.007","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) affects ∼30% of the global population and is associated with increased risks of heart failure (particularly heart failure with preserved ejection fraction), atrial fibrillation, and cardiovascular mortality. Despite well-established epidemiological links between MASLD and cardiovascular disease, the molecular pathways driving MASLD-related cardiac remodeling remain incompletely understood. This state-of-the-art mini review examines ferroptosis and pyroptosis as potentially convergent regulated cell-death pathways relevant to both the steatotic liver and the remodeling heart. Ferroptosis is an iron-dependent, lipid peroxidation-driven cell death that mediates hepatocyte injury in experimental MASLD and contributes to cardiomyocyte injury under cardiac stress. Pyroptosis is an inflammasome-mediated pro-inflammatory cell death executed by gasdermin D, which amplifies tissue inflammation in hepatic and cardiac disease. Direct preclinical evidence from a pressure-overload heart-failure model demonstrates ferroptosis-to-pyroptosis signaling through the ACSL4/ALOX12/12-HETE/NLRP3 axis; however, this cascade has not yet been directly validated in MASLD models or in patients with MASLD-associated cardiac remodeling. We therefore distinguish experimentally established within-organ mechanisms from hypothesized interorgan liver-heart links, highlight shared regulators including reactive oxygen species, the cGAS/STING pathway, and the NRF2 hub, and discuss translational strategies and evidence gaps that should guide future validation.</p>","PeriodicalId":94257,"journal":{"name":"Translational research : the journal of laboratory and clinical medicine","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149229580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological Neutralization of the Rspo2/Wnt Axis Preserves Subchondral Bone Plate and Vascular Niche Integrity to Attenuate Cartilage Degeneration in Osteoarthritis.","authors":"Dong Guo, Lingfeng Yang, Xin Liu, Xiaozhuan Wang, Fengtian Sun, Anbiao Zhang, Xinya Lu, Yongzhi Lin, Zhigang Zhong, Xiaoshuai Wang, Chuangxin Lin","doi":"10.1016/j.trsl.2026.10.005","DOIUrl":"https://doi.org/10.1016/j.trsl.2026.10.005","url":null,"abstract":"<p><strong>Objectives: </strong>Osteoarthritis (OA) involves the structural failure of the joint unit, where the subchondral bone plate and associated vascular niche serve as a critical barrier and mechanical support for articular cartilage. This study investigates R-spondin 2 (Rspo2) as a mediator of instability within the subchondral bone plate-associated vascular niche and evaluates whether its pharmacological neutralization attenuates niche disruption and preserves osteochondral integrity.</p><p><strong>Method: </strong>Human tibial-plateau subchondral bone scRNA-seq (GSE196678) and clinical specimens were analyzed to identify Wnt-related pathways. OA was induced in mice via ACLT+DMM surgery. Weekly intra-articular administration of recombinant Rspo2, an Rspo2-neutralizing antibody (Rspo2-NAb), or the Wnt inhibitor DKK1 began on postoperative day 3. Subchondral bone remodeling and cartilage degeneration were assessed in separate groups of mice at postoperative days 30 and 60.</p><p><strong>Results: </strong>The scRNA-seq analysis identified Wnt-related expression patterns in OA subchondral endothelial cells (ECs). Histology showed a higher percentage of CD31⁺/p-β-catenin (Ser675)⁺ cells in OA specimens than in controls. In vitro, rhRspo2 enhanced endothelial proliferation and tube formation, whereas conditioned medium from Rspo2-overexpressing ECs promoted osteogenic and osteoclastic differentiation and disrupted chondrocyte homeostasis; these effects were attenuated by Rspo2-NAb or DKK1, consistent with involvement of Wnt/β-catenin signaling. Early postoperative administration of Rspo2-NAb or DKK1 reduced subchondral bone plate remodeling and the proportion of CD31⁺EMCN⁺ cells, and attenuated cartilage degeneration in vivo.</p><p><strong>Conclusions: </strong>These findings support a paracrine role for endothelial-derived Rspo2 in vitro and the potential of early Rspo2 neutralization to attenuate bone remodeling and cartilage degeneration in experimental OA.</p>","PeriodicalId":94257,"journal":{"name":"Translational research : the journal of laboratory and clinical medicine","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149198600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ocular Immune Toxicity in Cancer Immunotherapy, From Immune Privilege Breakdown to Treatment Rechallenge: A Review.","authors":"Kai-Yang Chen, Hoi-Chun Chan, Michael Lim, Chi-Ming Chan","doi":"10.1016/j.trsl.2026.10.004","DOIUrl":"https://doi.org/10.1016/j.trsl.2026.10.004","url":null,"abstract":"<p><p>Immune checkpoint inhibitors (ICIs) have transformed cancer therapy but can disrupt ocular immune privilege and produce heterogeneous immune-related adverse events (Eye-irAEs). This structured narrative review with evidence mapping integrates clinical, epidemiologic, mechanistic, pharmacovigilance, and management data to define translational pathways from checkpoint blockade to ocular toxicity and treatment decisions. In a real-world cohort of 41,020 ICI-treated patients, ophthalmic irAEs occurred in 4.18% within 1 year, including dry eye disease in 2.00%, conjunctivitis in 0.87%, blepharitis in 0.51%, anterior uveitis in 0.39%, and keratitis in 0.38%. A 2026 meta-analysis of five cohorts comprising 277,790 participants found increased uveitis risk with ICI exposure (hazard ratio 2.26), while pooled overall survival was not significantly associated with ICI-related uveitis (hazard ratio 0.69, 95% CI 0.35-1.39). Among patients with preexisting uveitis, recurrence reached 38.9% for prior anterior disease and 51.1% for prior intermediate, posterior, or panuveitis. Risk varies by malignancy and regimen; melanoma was associated with substantially greater noninfectious uveitis than lung cancer (1.10% vs 0.18%; risk ratio 6.17, 95% CI 4.20-9.08). Mechanistically, PD-1/PD-L1 and CTLA-4 have the strongest established exposure-toxicity evidence, LAG-3 signals are emerging, and TIM-3 and TIGIT remain translational. Phenotype-directed local or systemic therapy can preserve vision and permit ICI continuation or rechallenge in selected patients. In a 2026 rechallenge series, four of five rechallenged patients had no documented recurrence, while one recurrence resolved successfully with corticosteroid treatment. Standardized phenotyping, longitudinal ophthalmic surveillance, multidisciplinary attribution, and prospective ocular endpoints should translate mechanistic insight into safer immunotherapy, individualized rechallenge, and improved cancer-treatment continuity.</p>","PeriodicalId":94257,"journal":{"name":"Translational research : the journal of laboratory and clinical medicine","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149198635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The key role of cellular plasticity in the development of colorectal cancer.","authors":"Lingqiao Lou, Yanghui Cao, Zhiyuan Ma, Bei Ji, Shuhui Liu, Kenichi Mizuno, Shuji Terai, Biguang Tuo, Taolang Li, Xuemei Liu","doi":"10.1016/j.trsl.2025.12.002","DOIUrl":"10.1016/j.trsl.2025.12.002","url":null,"abstract":"<p><p>The development of colorectal cancer, which is a malignant tumor demonstrating high morbidity and mortality worldwide, involves complex molecular mechanisms and biological processes. Early-stage colorectal cancer patients do not exhibit obvious clinical symptoms; thus, they are often diagnosed with middle-stage to late-stage disease. The overall survival of advanced colorectal cancer patients with metastasis and treatment resistance is poor. Notably, tumor cell plasticity promotes tumorigenesis, metastasis, and therapeutic resistance, thus leading to the high incidence and mortality of colorectal cancer. In-depth studies of cellular plasticity are expected to lead to the identification of new therapeutic targets. In this review, we systematically summarize the role of cellular plasticity in colorectal cancer development and explore the regulatory mechanisms associated with cellular plasticity in colorectal cancer, with the aim of providing a theoretical basis for the development of innovative therapeutic strategies for this type of cancer.</p>","PeriodicalId":94257,"journal":{"name":"Translational research : the journal of laboratory and clinical medicine","volume":" ","pages":"40-47"},"PeriodicalIF":5.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145696470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intermittent caloric restriction protects against diabetic heart inflammation via GSDMD-dependent sFRP2-ATF6-NF-κB pathway.","authors":"Kaibin Lin, Changlin Zhai, Ai Wang, Yang Lan, Yun Zhao, Qiwei Zhai, Junbo Ge, Yan Yan","doi":"10.1016/j.trsl.2025.05.006","DOIUrl":"10.1016/j.trsl.2025.05.006","url":null,"abstract":"<p><strong>Background: </strong>Calorie restriction holds the potential in alleviating metabolic disorders and inflammation. However, the effects of intermittent caloric restriction (ICR) on cardiometabolic diseases remain poorly understood. In this study, we aimed to assess the protective role of ICR in both prediabetic and diabetic heart injury.</p><p><strong>Methods: </strong>Prediabetic and diabetic models were established using a high-fat diet and high-fat diet/streptozotocin in mice, respectively. Following the induction of prediabetes mellitus and diabetes mellitus, ICR was implemented to evaluate its therapeutic effect. As alterations of gasdermin D (GSDMD) expression were monitored, we investigated the relationship between the cardioprotective effect of ICR and GSDMD using human heart samples, GSDMD knockout mice and adeno-associated virus 9(AAV9). Through RNA-sequencing, the underlying mechanism of GSDMD-mediated diabetes-associated cardiac inflammation was further elucidated.</p><p><strong>Results: </strong>Our study indicated that ICR prevented cardiac dysfunction by alleviating cardiac lipid overaccumulation in prediabetic mice. Conversely, the effect of ICR on lipid overaccumulation were limited in diabetic mice. Instead, the cardioprotective effect of ICR was mediated through the inhibition of GSDMD-mediated cardiomyocyte pyroptosis and inflammation response in diabetic mice. In human hearts, the expression level of GSDMD were positively correlated with diabetes-induced heart injuries. Furthermore, GSDMD deficiency mimicked the cardioprotective effects of ICR, while GSDMD overexpression in cardiomyocytes offset the cardioprotective effect of ICR in diabetic mice. Mechanistically, the upregulation of GSDMD activated secreted Frizzled-related protein 2 (sFRP2)/ATF6/NF-κB pathway, exacerbating cardiac inflammation in diabetic hearts. Moreover, the replenishment of recombinant sFRP2 offset the cardiac benefits of GSDMD deficiency in diabetic mice.</p><p><strong>Conclusions: </strong>Our study demonstrated the prevention of prediabetic and diabetic heart injury by ICR were mediated by alleviating cardiac lipid overaccumulation and inflammation, respectively. Moreover, targeting GSDMD-dependent sFRP2/ATF6/ NF-κB pathway conferred the cardioprotective effects of ICR and could serve as a potential therapeutic strategy for diabetic heart failure.</p>","PeriodicalId":94257,"journal":{"name":"Translational research : the journal of laboratory and clinical medicine","volume":" ","pages":"59-76"},"PeriodicalIF":5.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144210617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hierarchical multimodal structural and material analysis of bone in diabetes.","authors":"Ashu Rastogi, Raveena Singh, Saroj Kumar, Srinivas Seshabhattaru, Rajesh Kesavan, Uttam Chand Saini, Navin Kumar, Sanjay Kumar Bhadada","doi":"10.1016/j.trsl.2025.11.004","DOIUrl":"10.1016/j.trsl.2025.11.004","url":null,"abstract":"<p><strong>Objective: </strong>Diabetic neuropathy and Charcot neuroarthropathy (CN) may compromise lower limb skeletal integrity. We performed a comprehensive comparative assessment of foot bone across multiple hierarchical parameters at nano, meso and micro scale orders.</p><p><strong>Research design and methods: </strong>Calcaneal bone specimens obtained from individuals with CN (Group A; n = 12), diabetic neuropathy (Group B; n = 21), and healthy controls (Group C; n = 18). Trabecular microarchitecture was assessed using micro-computed tomography (micro-CT), mechanical strength through uniaxial compression, biochemical composition by infrared spectroscopy (FTIR), crystal dimensions with X-ray diffraction (XRD), tissue-level mechanical behaviour by nanoindentation and quantiative organic and mineral content of bone matrix by thermogravimetric analysis (TGA).</p><p><strong>Results: </strong>Micro-CT revealed 35.9 % reduced trabecular thickness (0.25 ± 0.11 mm vs 0.39 ± 0.14 mm, p = 0.016), 57 % lower maximum load tolerance (218.85 ± 18.84 N vs 508.15 ± 100.98 N, p < 0.001) and 55 % reduced stiffness (51.62 ± 4.89 N/mm vs. 114.63 ± 13.74 N/mm, p < 0.001) in Group A compared to Group C, respectively. Mineral-to-matrix ratio (3.17 ± 0.68 vs. 4.75 ± 1.47, p < 0.001), collagen maturity index (1.25± 0.29 vs. 1.74 ± 0.50, p < 0.001) and organic fraction (44.95 ± 5.15 % vs 50.91 ± 4.85 %;p = 0.005) were lower in Group A compared to group C, respectively. The elastic modulus (8.13 ± 1.57 GPa vs. 18. 12± 1.96 GPa) and hardness (0.34 ± 0.07 GPa vs. 0.71 ± 0.13 GPa) were significantly reduced in group A compared to Group C (p < 0.001 for both), confirming compromised tissue-level mechanics of foot bones in CN. Bone samples from Group B showed intermediate values compared to either group A and C, respectively.</p><p><strong>Conclusion: </strong>Charcot neuroarthropathy of foot is characterised by severe, multiscale impairments in bone architecture, composition, and mechanical function that contribute to heightened skeletal fragility and underscore the need for targeted interventions addressing bone quality.</p>","PeriodicalId":94257,"journal":{"name":"Translational research : the journal of laboratory and clinical medicine","volume":" ","pages":"1-11"},"PeriodicalIF":5.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145644389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the ApoB100-ENO1 interaction with engineered peptides attenuates atherosclerotic inflammation and plaque progression.","authors":"Hyun Jung Yoo, Dan Hoang Nguyet Vo, Shin Eui Kang, Sang Jin Lee, Shindy Soedono, Esther Jin Joo, Maria Averia, Kae Won Cho, Yeong Wook Song","doi":"10.1016/j.trsl.2025.12.003","DOIUrl":"10.1016/j.trsl.2025.12.003","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis, a chronic inflammatory disease, presents significant \"residual risk\" even with effective lipid-lowering therapies, primarily due to persistent vascular inflammation. Apolipoprotein B100 (ApoB100) acquires pro-inflammatory properties upon modification and binds to cell-surface enolase 1 (ENO1), an immune modulator upregulated in inflammatory conditions. This interaction induces inflammatory responses via NF-κB activation. Targeting the ApoB100-ENO1 interaction may offer a novel strategy to reduce vascular inflammation and atherosclerosis progression.</p><p><strong>Methods: </strong>We developed PP3m, a stabilized ApoB100-derived peptide, to selectively inhibit the ApoB100-ENO1 interaction. Single-cell RNA sequencing (scRNA-seq) data from human atherosclerotic plaques were reanalyzed to characterize ENO1 expression in myeloid cells. In vitro, PP3m's anti-inflammatory effects were evaluated across various macrophage models stimulated by diverse inflammatory stimuli. Outcomes included cytokine secretion, inflammatory gene expression, foam cell formation, oxidized low-density lipoprotein (oxLDL) uptake, and signaling pathways activation. In vivo, Ldlr^-/- mice fed an atherogenic diet were treated with PP3m to evaluate its effects on atherosclerosis progression, macrophage accumulation, and systemic inflammation.</p><p><strong>Results: </strong>scRNA-seq analysis revealed that human atherosclerotic plaques harbor significantly more ENO1 macrophages, with ENO1 expression enriched in CD68⁺ M1 macrophages. Atherogenic stimuli induced ENO1 translocation to the plasma membrane in macrophages. In vitro, PP3m significantly attenuated inflammatory responses by suppressing IL-6 and CXCL8 secretion, reducing M1 polarization, and dose-dependently inhibiting oxLDL-induced foam cell formation and uptake. In vivo, PP3m reduced aortic lesion area, lipid content, and collagen deposition, accompanied by decreased macrophage accumulation in plaques and lower circulating pro-inflammatory cytokines. Importantly, these effects were independent of changes in plasma lipid profiles.</p><p><strong>Conclusions: </strong>The ApoB100-ENO1 axis is a critical driver of macrophage-mediated inflammation in atherosclerosis. The novel peptide PP3m effectively inhibits this interaction, reducing vascular inflammation and plaque progression without altering lipid levels. PP3m represents a promising therapeutic candidate for cardiovascular disease by targeting residual inflammatory risk through a lipid-independent mechanism.</p>","PeriodicalId":94257,"journal":{"name":"Translational research : the journal of laboratory and clinical medicine","volume":" ","pages":"28-39"},"PeriodicalIF":5.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145710672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neutrophil-derived exosomal thrombospondin-1 exacerbates endothelial progenitor cell senescence and lung injury via TGF-β/SMAD signaling in COPD.","authors":"Junjuan Lu, Caihong Liu, Ting Yuan, Honghui Yang, Li Zhang","doi":"10.1016/j.trsl.2025.12.004","DOIUrl":"10.1016/j.trsl.2025.12.004","url":null,"abstract":"<p><strong>Background: </strong>Chronic obstructive pulmonary disease (COPD) is a chronic respiratory condition primarily caused by inhalation of harmful particles such as tobacco smoke. Cellular senescence serves as a key driver in its pathogenesis. Although endothelial progenitor cells (EPCs) have been shown to alleviate COPD by reducing inflammatory cell infiltration, the role and mechanisms underlying EPC senescence in this disease remain unclear.</p><p><strong>Methods: </strong>A cigarette smoke (CS)-exposed COPD mouse model was established. Lung injury was assessed histologically, with concurrent quantification of neutrophil infiltration and cellular senescence levels in lung tissues. Pearson analysis evaluated the correlation between senescence severity and neutrophil numbers. In vivo neutrophil depletion was achieved using anti-Ly6G antibody, while GW4869 was used to inhibit exosome secretion from COPD-derived neutrophils. Neutrophils were then co-cultured with EPCs to assess their impact on EPC senescence and DNA damage. Proteomic analyses were employed to identify mechanisms of neutrophil-derived exosomes in COPD.</p><p><strong>Results: </strong>COPD mice exhibited significant lung tissue damage, accelerated cellular senescence, and increased neutrophil infiltration. Senescence severity positively correlated with neutrophil proportion. Mechanistically, thrombospondin-1 (TSP-1) was highly expressed in COPD-derived neutrophils. Knockdown of neutrophil-derived exosomal TSP-1 alleviated EPC senescence. Furthermore, TSP-1 expression was regulated by transcription factor FOS, whereas TGF-β inhibition attenuated the promoting effects of TSP-1 overexpression on cellular senescence and lung injury in COPD mice.</p><p><strong>Conclusion: </strong>This study demonstrates that neutrophil-derived exosomal TSP-1 aggravates EPC senescence and lung injury in COPD, revealing the pathogenic role of TSP-1 in disease progression and highlighting its potential as a therapeutic target.</p>","PeriodicalId":94257,"journal":{"name":"Translational research : the journal of laboratory and clinical medicine","volume":" ","pages":"12-27"},"PeriodicalIF":5.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145784237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ZONAB regulates renal cyst formation in nphp1 knockout mice.","authors":"Jiayong Lai, Xiaoya Wei, Dantong Li, Xiaohong Wu, Yaqing Liu, Huamu Chen, Zhihui Yue, Liangzhong Sun","doi":"10.1016/j.trsl.2025.12.001","DOIUrl":"10.1016/j.trsl.2025.12.001","url":null,"abstract":"<p><p>Tubular dilation and cyst formation at the corticomedullary junction are distinct pathological features of nephronophthisis (NPH) and may be associated with disease progression. However, the mechanism of renal cyst formation in NPH is unclear. Increased cell proliferation is necessary for cyst formation. ZONAB, a tight junction-associated transcriptional regulatory factor, targets proliferative factors, such as CCND1 and PCNA. In this study, we explored the role of ZONAB in renal cyst formation and its possible mechanism in nphp1 knockout (nphp1^KO) mice. We found that the expression of ZONAB, CCND1, and PCNA was increased in the kidney tissue of the nphp1^KO mice but was mainly confined to renal cyst cells. ZONAB knockdown inhibited renal cyst formation and tubular dilatation and decreased the expression of CCND1 and PCNA in the nphp1^KO mice. We concluded that ZONAB plays an important role in renal cyst formation in the NPH, possibly through the regulation of CCND1 and PCNA.</p>","PeriodicalId":94257,"journal":{"name":"Translational research : the journal of laboratory and clinical medicine","volume":" ","pages":"48-58"},"PeriodicalIF":5.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145703689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Exosomal Tenascin-C primes macrophage pyroptosis amplifying aberrant inflammation during sepsis-induced acute lung injury\" [Translational Research 270 (2024) 66-80].","authors":"Ting Gong, Xuedi Zhang, Xiaolei Liu, Yinfeng Ye, Zhiyuan Tian, Shuang Yin, Min Zhang, Jing Tang, Youtan Liu","doi":"10.1016/j.trsl.2025.08.001","DOIUrl":"10.1016/j.trsl.2025.08.001","url":null,"abstract":"","PeriodicalId":94257,"journal":{"name":"Translational research : the journal of laboratory and clinical medicine","volume":"283 ","pages":"1-2"},"PeriodicalIF":5.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}