Bioscience trends最新文献

{"title":"Pathways to embed digital health technologies and their governance mechanisms in Long-Term Care Insurance Systems: A comparative review of Japan, South Korea, and China.","authors":"Yuhan Cheng, Yue Han, Li Wang, Jiajia Ma, Kenji Karako, Yan Shi, Peipei Song","doi":"10.5582/bst.2026.01098","DOIUrl":"https://doi.org/10.5582/bst.2026.01098","url":null,"abstract":"<p><p>Rapid population aging is increasing demand for long-term care (LTC), prompting many countries to institutionalize financing and service provision through long-term care insurance (LTCI). Digital health technologies are increasingly embedded into LTCI, and yet the pathways in which they are embedded and their governance effects differ across institutional contexts. This comparative review synthesizes evidence from Japan, South Korea, and China across five operational domains-institutional foundations, eligibility determination, service management, fund oversight, and policy steering-and uses a sociotechnical systems lens to analyze how technology and institutions co-evolve. We propose a three-layer model of institutional embedding linking welfare-boundary constraints, governance mechanisms shaping data-driven operations, and path dependence in policy and implementation. In the three countries, digital health technologies have not fundamentally expanded the welfare boundary of LTCI, but they have reshaped how LTCI is administered, shifting i) needs assessment from experience-led judgment toward data-driven decision-making support, ii) service management from flexible discretion toward rules and platform-based coordination, and iii) oversight from ex post auditing toward process-oriented monitoring. Distinct national pathways have emerged: a supplementary-technology pathway in Japan, a state-led integration pathway in South Korea, and an exploratory co-evolutionary pathway in China. These benefits are accompanied by practical risks, including algorithmic bias, inconsistent data quality, privacy and security concerns, and potential erosion of institutional flexibility. The proposed model helps explain cross-national divergence and provides a governance-oriented basis for selecting embedding strategies and safeguards in different LTCI contexts.</p>","PeriodicalId":8957,"journal":{"name":"Bioscience trends","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147760678","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":"Comparative safety and efficacy of BIC/FTC/TAF versus DTG+3TC in antiretroviral treatment-naive patients with HIV as first-line regimens: A real-world cohort study.","authors":"Liqin Sun, Yuxin Jiang, Stephane Isnard, Jingyi Chen, Yanjun Li, Hui Wang, Fang Zhao, Man Rao, Xinyun Jia, Jinping Huang, Jinwei Wu, Yinsong Luo, Dian Zhao, Chenye Liu, Xiaorui Li, Jean-Pierre Routy, Jiaye Liu, Yun He, Ping Cen, Hongzhou Lu","doi":"10.5582/bst.2025.01335","DOIUrl":"https://doi.org/10.5582/bst.2025.01335","url":null,"abstract":"<p><p>While bictegravir/emtricitabine/tenofovir alafenamide (BIC/FTC/TAF) and dolutegravir plus lamivudine (DTG+3TC) are first-line regimens for treatment-naive people with HIV (PWH), long-term real-world head-to-head comparisons of their metabolic and renal outcomes remain limited. We conducted a retrospective cohort study of ART-naive PWH initiating these regimens in China, utilizing 1:2 propensity score matching (PSM) to balance baseline covariates for 1,445 participants (901 BIC/FTC/TAF; 544 DTG+3TC). Over a 24-month follow-up, the study demonstrated comparable virologic suppression (99.7% vs. 100.0%; p = 0.623), weight changes, and cumulative incidence of metabolic abnormalities between the two groups. Conversely, although the crude 24-month incidence of eGFR decline was higher with DTG+3TC (54.8% vs. 40.7%; p = 0.039), adjusted Cox models revealed that the regimen was not independently associated with this decline (HR 1.20; 95% CI 0.97-1.48; p = 0.18).These findings indicate that both regimens offer comparable long-term virologic efficacy and metabolic safety profiles, supporting their routine clinical utility while highlighting the need for cautious interpretation of renal markers during integrase inhibitor-based therapy.</p>","PeriodicalId":8957,"journal":{"name":"Bioscience trends","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147760675","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":"Liver transplantation in Japan: Achievements, limitations, and future perspectives.","authors":"Yasuhiko Sugawara","doi":"10.5582/bst.2026.01094","DOIUrl":"https://doi.org/10.5582/bst.2026.01094","url":null,"abstract":"<p><p>Liver cirrhosis (LC) represents a substantial and growing global health burden, driving high mortality through liver failure and hepatocellular carcinoma (HCC), for which liver transplantation (LT) remains the only definitive and life-saving therapy. Despite continuous technical and perioperative advances, a critical unmet need persists due to the imbalance between organ demand and availability. In Japan, the practice of LT is uniquely shaped by the predominance of living donor transplantation and a marked epidemiological transition: the burden of viral hepatitis-related cirrhosis has declined with antiviral therapies, while metabolic dysfunction-associated steatohepatitis (MASH) and alcohol-associated liver disease (ALD) are emerging as leading indications. This paradigm shift necessitates refinement of transplant strategies, including improved candidate selection for HCC through integration of tumor biology and novel biomarkers and careful consideration of immunotherapy-related risks. Moreover, MASH introduces complex challenges related to obesity, disease recurrence, and the role and timing of metabolic interventions, whereas ALD raises ongoing clinical and ethical questions regarding early transplantation and relapse prevention. Future progress will depend on expanding the donor pool through innovations such as machine perfusion and xenotransplantation as well as expanding indications to selected non-HCC malignancies and adopting advanced surgical technologies. Collectively, LT is transitioning toward a precision-based, multidisciplinary, and innovation-driven paradigm.</p>","PeriodicalId":8957,"journal":{"name":"Bioscience trends","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721731","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":"Modeling of the hepatitis B virus life cycle and the efficacy of antivirals in human iPSC-derived hepatic organoids.","authors":"Tanbin Liu, Junming Xu, Xiaoni Chen, Jingyi Li, Jie Ke, Jiasen Xu, Hongzhou Lu, Fenfang Wu","doi":"10.5582/bst.2026.01043","DOIUrl":"https://doi.org/10.5582/bst.2026.01043","url":null,"abstract":"<p><p>Hepatitis B virus (HBV) infection remains a major global health burden, affecting approximately 296 million people worldwide, and yet progress in mechanistic studies and development of antivirals has been limited by the lack of physiologically relevant and sustainable in vitro models. This study established a human induced pluripotent stem cell (hiPSC)-derived multilineage hepatic organoid system that robustly supports the complete HBV life cycle, including viral entry, replication, covalently closed circular DNA (cccDNA) formation, antigen secretion, and production of infectious progeny virus. These organoids exhibit stable expression of sodium taurocholate cotransporting polypeptide (NTCP), a key receptor for HBV entry, and remain viable long term under infection conditions for at least 20 days, with sustained secretion of HBsAg and HBeAg. Importantly, the model recreates key pathological features of chronic HBV infection, including downregulation of hepatocyte functional genes (e.g., ALB and CYP3A4) and induction of fibrosis-associated markers such as COL1A1, reflecting early extracellular matrix remodeling. Moreover, results indicated the utility of this platform in the evaluation of antivirals. Treatment with tenofovir effectively reduced viral DNA and antigen production without affecting cccDNA levels, whereas bulevirtide resulted in stage-specific inhibition of viral entry, highlighting the model's capacity to resolve mechanism-of-action differences. At the same time, drug-induced hepatotoxicity was assessed within the same system. Collectively, this hiPSC-derived hepatic organoid model provides a scalable and physiologically relevant platform that bridges the gap between conventional cell culture and in vivo systems, offering a powerful tool for studying HBV pathogenesis, host-virus interactions, and preclinical antiviral discovery.</p>","PeriodicalId":8957,"journal":{"name":"Bioscience trends","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509510","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":"Biallelic inactivation of EXT1 in patient-derived iPSCs confirms the \"Two-hit\" hypothesis in hereditary multiple osteochondromas.","authors":"Yali Yang, Zhenzhong Han, Guowei Li, Zihan Li, Chonghao Shao, Wentao Li, Jing Wang, Jing Luan, Yazhou Cui, Jinxiang Han","doi":"10.5582/bst.2026.01046","DOIUrl":"https://doi.org/10.5582/bst.2026.01046","url":null,"abstract":"<p><p>Hereditary Multiple Osteochondromas (HMO) is a rare autosomal dominant skeletal disorder caused by heterozygous loss-of-function mutations in EXT1 or EXT2, which encode glycosyltransferases essential for heparan sulfate (HS) biosynthesis. Whether haploinsufficiency alone suffices or biallelic inactivation is required for osteochondroma formation remains a central unresolved question. In this study, we employed CRISPR/Cas9 combined with PiggyBac transposon technology to introduce a second pathogenic mutation (c.1883+1G>T) into patient-derived induced pluripotent stem cells (iPSCs) carrying a heterozygous EXT1 c.1126C>T mutation. This approach enabled the generation of isogenic iPSC lines: wild-type (WT), single-mutant (SM), and double-mutant (DM). These iPSCs were differentiated through induced mesenchymal stem cells (iMSCs) into chondrocytes. Biallelic EXT1 mutation in DM cells led to significant upregulation of SOX9, COL2A1, and ACAN, elevated glycosaminoglycan (GAG) levels, and markedly reduced HS, whereas SM cells remained indistinguishable from WT. Three-dimensional (3D) chondrogenic organoid cultures revealed that DM organoids were enlarged and structurally disorganized, partially recapitulating key histopathological features of osteochondromas. Transcriptomic analysis identified the Wnt signaling pathway as the most significantly enriched pathway among differentially expressed genes following EXT1 loss. Collectively, these findings provide direct human cellular evidence that complete EXT1 inactivation-not haploinsufficiency-drives aberrant chondrogenesis, likely through impaired sequestration of morphogen ligands, thereby supporting the Two-hit pathogenic model.</p>","PeriodicalId":8957,"journal":{"name":"Bioscience trends","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509499","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":"Characteristics and management of constitutional indocyanine green excretory defect.","authors":"Jiaao Wang, Ziqi Hou, Jun Ji, Ding Hu, Changlong Wei, Zhihong Zhang, Yuanzhi Zhou, Haichuan Wang, Jiwei Huang","doi":"10.5582/bst.2026.01032","DOIUrl":"https://doi.org/10.5582/bst.2026.01032","url":null,"abstract":"<p><p>Indocyanine green (ICG) test is a popular and widely implied assessment of hepatic functional reserve (HFR) due to its safety and efficiency. However, as the application of ICG expanded, an exceedingly rare disorder, the constitutional ICG excretory defect (CIED), gradually emerged. CIED is considered as a harmless dye excretory defect, which features remarkable ICG plasma retention (plasma ICG 15-min retention rate is higher than 50%) without any severe liver impairments. Previous investigations revealed that it has no particular symptoms and it is not a contraindication of surgical treatments. The deficiency of the organic anion transporting polypeptide 1B3 is affirmed to be the underlying cause of CIED. It is of great significance to identify this disorder from other reasons elevating ICG-R15 and provide such patients with effective and safe treatments. The utility of ^99mTc-GSA liver scintigraphy, Child-Pugh and ALBI scores, and liver biopsy in identification and supplementary HFR assessment in CIED has been affirmed. Moreover, other methods based on radioactive tracers, serum biomarkers and imaging examinations have potential. Based on existing evidence, we proposed a clinical strategy that prioritizes ALBI and Child-Pugh scores, as well as imaging examinations, such as computerized tomography and ultrasound examinations, for the initial identification of CIED. Thereafter, ^99mTc-GSA liver scintigraphy or biopsy is used to verify CIED and assess HFR. In conclusion, we comprehensively reviewed the characteristics, mechanisms and coping strategies of CIED, aiming to provide updated insights of this disorder.</p>","PeriodicalId":8957,"journal":{"name":"Bioscience trends","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509546","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":"The orchestrated network of skin photoaging: From intercellular crosstalk to molecular signaling.","authors":"Bingmin Li, Cong Ren, Lixia Zhang, Weijie Gu","doi":"10.5582/bst.2026.01042","DOIUrl":"https://doi.org/10.5582/bst.2026.01042","url":null,"abstract":"<p><p>Photoaging is a distinct form of pathological skin aging driven primarily by chronic ultraviolet (UV) radiation, which clinically manifests as wrinkles, dyspigmentation, and loss of elasticity. Although core molecular events induced by UV-such as oxidative stress and DNA damage-are relatively well-understood, there is still a lack of a systematic and integrated understanding of how diverse cell types in the skin collectively drive photoaging through complex interactive networks. This review systematically elaborates the cellular and molecular mechanisms underlying skin photoaging. The key pathways involved are examined, including oxidative stress, apoptosis, dysregulated autophagy, activation of inflammatory cascades, and degradation of the extracellular matrix (ECM). This review further details the pivotal roles of and reciprocal crosstalk among fibroblasts, keratinocytes, melanocytes, and various immune cells. By providing an integrated perspective on these interactions, this review outlines the cellular and molecular mechanism of UV-associated senescence, which uniquely integrates the roles of the immune microenvironment and cellular crosstalk, providing a roadmap for next-generation anti-photoaging strategies.</p>","PeriodicalId":8957,"journal":{"name":"Bioscience trends","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147497658","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":"Allele-specific effects of distinct SLC26A4 variants on cochlear function and transcriptomic programs in compound heterozygous models.","authors":"Yue Li, Yiding Yu, Yan Zhao, Lin Deng, Jinge Xie, Shan Gao, Ying Li, Qingjia Cui, Shuo Wang, Lihui Huang","doi":"10.5582/bst.2026.01058","DOIUrl":"https://doi.org/10.5582/bst.2026.01058","url":null,"abstract":"<p><p>SLC26A4 is a major causative gene for hereditary hearing loss, its mutation spectrum shows pronounced population specificity. In Chinese populations, patients predominantly carry biallelic mutations, and compound heterozygous genotypes are prevalent, which results in a wide spectrum of auditory phenotypes. However, how different alleles interact within these contexts to shape phenotypic variability remains poorly understood. We employed cellular and mouse models to explore the allele-specific mechanisms associated with two novel mutations, a frameshift mutation and a missense mutation, in compound heterozygous that share the same splice-site pathogenic allele. In vitro, wild-type (WT) and mutant (c.574delC, c.1211C>A) SLC26A4 constructs were expressed in HeLa cells to assess pendrin localization. Both mutations reduced membrane enrichment and increased intracellular retention. In vivo, compound heterozygous knock-in mouse models (Slc26a4^{c.574delC/c.919-2A>G} and Slc26a4^{c.1211C>A/c.919-2A>G}) were generated using CRISPR/Cas9. The auditory function and cochlear pathology were investigated. Both compound mutants exhibited elevated ABR thresholds, with more severe hearing loss in Slc26a4^{c.574delC/c.919-2A>G} mice. Correspondingly, these mice showed marked hair cell disruption, stereociliary loss, and cochlear structural abnormalities, whereas the Slc26a4^{c.1211C>A/c.919-2A>G} mice displayed milder changes. Transcriptomic profiling examined by bulk RNA-sequencing revealed broader differential expression in Slc26a4^{c.574delC/c.919-2A>G} mice, enriched in structural and developmental pathways, while the missense model showed predominantly immune-related signatures. Our findings demonstrate that allele-specific functional divergence in compound heterozygous SLC26A4 mutations leads to distinct auditory dysfunction, cochlear pathology, and transcriptional programs. These findings provide mechanistic insight into the phenotypic heterogeneity of hearing loss and may indicate future allele-specific interventions or therapeutic strategies.</p>","PeriodicalId":8957,"journal":{"name":"Bioscience trends","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147497716","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":"The ATF5-GPER1 axis drives female protection in hepatocellular carcinoma through dual tumor-suppressive and immune-modulatory mechanisms.","authors":"Zhiquan Xu, Hao Wang, Qiang He, Hongshuai Cui, Zhongjun Wu, Rui Liao","doi":"10.5582/bst.2026.01026","DOIUrl":"https://doi.org/10.5582/bst.2026.01026","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) exhibits marked sexual dimorphism, with females demonstrating superior survival, yet the underlying molecular mechanisms remain unclear. We integrated bulk transcriptomics (GSE39791, TCGA-LIHC, GSE14520) and single-cell RNA sequencing (five datasets, n = 58 patients, 238,982 cells) with machine learning (LASSO, SVM, random forest) to identify female-protective genes driving HCC disparities. Activating transcription factor 5 (ATF5) emerged as a female-protective gene with higher expression in females versus males across cohorts. Single-cell analyses revealed ATF5 defines a female-enriched, low-grade malignant subcluster with elevated apoptotic programs and reduced proliferative signaling, and pseudotime analysis showed coordinated ATF5-GPER1 downregulation during malignant progression (Spearman ρ = -0.52 and -0.48; both p < 0.001). In the immune compartment, ATF5 marked a female-enriched IFN-γ⁺ macrophage state with enhanced immunostimulatory programs and preferential CXCL9/10-CXCR3-mediated communication with CD8/NK cells. Mechanistically, ATF5 transcriptionally activates G protein-coupled estrogen receptor 1 (GPER1), forming an estrogen-responsive regulatory module that functionally suppresses proliferation, induces apoptosis (HepG2: 26.45% vs. 11.88%, p < 0.0001), and inhibits migration in a GPER1-dependent manner as demonstrated by rescue experiments. Tissue microarray validation (n = 167) confirmed high ATF5 expression predicts improved recurrence-free survival specifically in female patients (HR = 0.34, p = 0.040) but not males (p = 0.080). The ATF5-GPER1 axis represents a female-protective circuit operating through tumor-intrinsic suppression and immune remodeling, offering mechanistic insight into HCC sexual dimorphism and identifying ATF5 as a sex-specific prognostic biomarker with potential therapeutic implications.</p>","PeriodicalId":8957,"journal":{"name":"Bioscience trends","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147479728","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":"The dual role of TRPA1 in dextran sulfate sodium (DSS)-induced murine colitis: Suppression alleviates acute inflammation but exacerbates subacute disease.","authors":"Fangzhou Dou, Jing Li, Daoran Lu, Yueyi Sun, Shasha Hu, Jianjun Gao","doi":"10.5582/bst.2025.01302","DOIUrl":"10.5582/bst.2025.01302","url":null,"abstract":"<p><p>Ulcerative colitis (UC) is a chronic inflammatory bowel disease with limited treatment options. Transient receptor potential ankyrin 1 (TRPA1) has been implicated in inflammation and pain, but its role in UC remains a subject of debate. The current study investigated the effects of TRPA1 inhibition in both acute and subacute murine models of dextran sulfate sodium (DSS)-induced colitis. Genetic knockout of Trpa1 or pharmacological inhibition with A967079 significantly ameliorated inflammation in the acute model, reducing the disease activity index (DAI), colon shortening, histopathological damage, and TNF-α secretion from macrophages. In contrast, TRPA1 suppression exacerbated subacute colitis and worsened weight loss, DAI, colon shortening, and histopathology. Mechanistically, Trpa1 deletion promoted CD4+ T cell polarization toward the Th1 subtype in subacute colitis, increasing IFN-γ levels. These findings reveal a dual role for TRPA1 in colonic inflammation: it mediates pro-inflammatory effects primarily via innate immune cells in the acute phase but has anti-inflammatory effects by modulating adaptive immunity in the subacute phase. These findings provide new insights into the context-dependent roles of TRPA1 and suggest that TRPA1 may represent a context-specific and stage-dependent therapeutic target in UC.</p>","PeriodicalId":8957,"journal":{"name":"Bioscience trends","volume":" ","pages":"91-104"},"PeriodicalIF":5.0,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146046099","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}