Biology Direct最新文献

{"title":"The role of autophagy in ocular health: mechanisms, pathologies, and therapeutic strategies.","authors":"Mingyu Huang, Yumeng Lin, Hong Zhang, Ruimin Yuan, Liuzhi Zeng, Sizhen Li, Qingsong Yang, Meng Gong, Renyan Xiao, Peng Jia, Lan Yuan, Qian Guo, Zhongyu Han, Lidan Xie","doi":"10.1186/s13062-026-00821-4","DOIUrl":"https://doi.org/10.1186/s13062-026-00821-4","url":null,"abstract":"<p><p>Autophagy is a self-digestive process in which cellular components are degraded and recycled to maintain homeostasis and cope with stress. When cells are in a state of stress, autophagy will degrade proteins, lipids and damaged organelles, and convert them into key nutrients and building cornerstones needed to maintain cell homeosis. More and more evidence shows that there is a link between autophagy process damage and the development of a variety of ophthalmic diseases that seriously threaten vision, including age-related macular degeneration, glaucoma and the formation of cataracts. Through a systematic review, we integrate experimental data covering basic biological mechanisms, genetic models and clinical evidence to clarify these pathological associations. With a focus on the mechanisms and regulation of autophagy in various ocular tissues and diseases, we analyzed research on autophagy in the lens, retina, cornea, and trabecular meshwork. Key findings elucidate the specific mechanisms of autophagy in maintaining lens transparency, promoting retinal ganglion cell survival, and regulating ocular immunity, demonstrating its critical role in preserving cellular equilibrium in ocular tissues. Furthermore, we evaluated potential therapeutic strategies targeting autophagic pathways, including mammalian target of rapamycin (mTOR) inhibition, transcription factor EB(TFEB) activation, noncoding RNA regulation, gene editing, and artificial intelligence-assisted diagnostics, which show significant promise for modulating autophagy to treat ocular diseases. The results of this review underscore the importance of autophagy in ocular health and disease.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PPBP orchestrates autophagy-apoptosis imbalance to drive cartilage degeneration in osteoarthritis.","authors":"Han Zhang, Kehao Hou, Xiao Ma, Guantong Sun, Le Kuai, Tianrui Wang, Yongtao Zhang, Guanhong Chen, Xiaohong Huang, Yingze Zhang","doi":"10.1186/s13062-026-00822-3","DOIUrl":"10.1186/s13062-026-00822-3","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by progressive cartilage destruction, in which dysregulated chondrocyte apoptosis and impaired autophagy play critical roles, yet the upstream molecular drivers remain incompletely understood. Here, we identify pro-platelet basic protein (PPBP/CXCL7) as a previously unrecognized mediator of cartilage degeneration in OA. PPBP expression was markedly elevated in human OA cartilage, in the destabilization of the medial meniscus (DMM) mouse model, and in IL-1β-stimulated primary chondrocytes. Functional analyses revealed that PPBP overexpression augmented inflammatory and catabolic responses, suppressed autophagy, and promoted chondrocyte apoptosis, whereas PPBP knockdown preserved extracellular matrix homeostasis, enhanced LC3-associated autophagy, and reduced apoptotic cell death. Mechanistically, PPBP activation was associated with increased phosphorylation of PI3K and AKT and concomitant autophagy suppression; conversely, PPBP inhibition reduced PI3K and AKT phosphorylation, restored autophagic activity, and these protective effects were abolished by pharmacological autophagy inhibition using 3-methyladenine. Importantly, intra-articular silencing of PPBP in DMM mice attenuated cartilage erosion, preserved collagen II, reduced MMP13 expression, increased LC3 levels, and decreased chondrocyte apoptosis in vivo. Collectively, these findings establish PPBP as a key regulator of autophagy-apoptosis imbalance in OA chondrocytes and highlight PPBP as a potential therapeutic target for disease-modifying intervention in OA.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tetrahydropalmatine may alleviate doxorubicin-induced renal injury by activating the Sirt3-mediated Nrf2/HO-1 pathway.","authors":"Wei Wang, Yuanyuan Hu, Yan Xu, Ning Ding, Jiping Wei, Cairong Li, Yong Chen","doi":"10.1186/s13062-026-00773-9","DOIUrl":"https://doi.org/10.1186/s13062-026-00773-9","url":null,"abstract":"","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Carbomol hydrogels integrating chlorogenic acid-loaded exosomes promote diabetic wound healing through antibacterial and immunomodulatory activities.","authors":"Hehui Wang, Ming Guan, Guangyu Chu, Yue Wang","doi":"10.1186/s13062-026-00818-z","DOIUrl":"https://doi.org/10.1186/s13062-026-00818-z","url":null,"abstract":"<p><p>Diabetic wounds represent a significant global clinical challenge, exacerbated by persistent bacterial infection and a dysregulated inflammatory microenvironment. Effective strategies for diabetic wounds are absent. Here, we found that NOD-like receptor thermal protein domain associated protein 3 (NLRP3) is an important regulating molecule associated with inflammatory microenvironment. We engineered Carbomol hydrogels integrating chlorogenic acid-loaded exosomes (Exo-CA@CB) to address both infection and NLRP3-mediated inflammation. The Carbomol hydrogel (CB) matrix provides biocompatibility, adhesion, self-healing properties, and sustained release, while the encapsulated Exo-CA deliver bioactive cargo. In vitro studies demonstrated the potent antibacterial activity of Exo-CA@CB against common wound pathogens. Crucially, Exo-CA@CB effectively promoted macrophage polarization towards the regenerative M2 phenotype. In the infected diabetic wound model, topical application of Exo-CA@CB hydrogels significantly accelerated healing. This study validates a new approach, initiated by single-cell analysis, for developing Exo-CA@CB hydrogels as a promising platform to manage infected diabetic wounds by concurrently tackling infection and NLRP3-driven inflammation.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative transcriptomic profiling reveals NK cell exhaustion-associated prognostic genes and identifies CSF1 as a key immunoregulatory target in hepatocellular carcinoma.","authors":"Yu Wang, Xiaoyan Xu, Yu Qi, Yiling Zhang, Long Ding, Zhuang Li, Shuqin Long, Guohua Yang, Rui Sun, Xiaohong Guo","doi":"10.1186/s13062-026-00814-3","DOIUrl":"https://doi.org/10.1186/s13062-026-00814-3","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) features a complex tumor immune microenvironment (TIME) where natural killer cell exhaustion (NKEX) facilitates immune evasion. Its regulatory networks and prognostic value remain insufficiently understood.</p><p><strong>Methods: </strong>We integrated single-cell (GSE149614) and bulk RNA-seq (TCGA-LIHC) data. Following Seurat-based clustering, we utilized CellChat and pySCENIC for communication and transcription factor analysis. NKEX-associated modules were identified via gene set variation analysis and weighted gene co-expression network analysis. A prognostic signature was developed using LASSO-Cox regression and validated in an external cohort (ICGC). CSF1 was prioritized for validation through clinical immunohistochemistry, siRNA knockdown, and Western Blotting. Candidate compounds identified via reverse network pharmacology were validated through CCK-8 assays, docking, western blotting and quantitative PCR.</p><p><strong>Results: </strong>Single-cell analysis revealed pronounced NKEX and disrupted communication in HCC. A four-gene prognostic signature (AKR1B1, SMS, CSF1, CFL1) demonstrated robust predictive performance in both TCGA (1-year AUC: 0.759) and external validation cohorts. High-risk patients showed significantly poorer survival. CSF1 was markedly upregulated in HCC tissues; its silencing inhibited Huh7 cell migration and invasion while upregulating CXCL10 in Huh7 cells and CXCR3 in NK92 cells. Molecular docking and CCK-8 assays justified the dosage and identified punicalagin and evoden as potent inhibitors that significantly suppressed CSF1 expression at both mRNA and protein levels.</p><p><strong>Conclusion: </strong>Through integrated multi-omics and experimental validation, we characterized NKEX in HCC and established a robust prognostic signature. CSF1 emerged as a key immunomodulatory target. Punicalagin and evoden were identified as potential lead compounds to modulate the CSF1, offering a promising strategy to restore antitumor immunity in HCC.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147762074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ALDH2 inhibits FASN stabilization via the E3 ligase CBL to suppress lipid accumulation and liver cancer development.","authors":"Yuxin Wang, Lu Li, Fanqi Qu, Tao Hua, Chu Chen, Lu Yang, Rong Jiang, Xuanke Liu, Pu Cheng, Hongxiao Min, Yixiang Wang, Xiucheng Pan, Dexu Sun, Renxian Tang, Ruyu Liu, Hongjuan You, Fanyun Kong","doi":"10.1186/s13062-026-00806-3","DOIUrl":"https://doi.org/10.1186/s13062-026-00806-3","url":null,"abstract":"","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of alternative splicing in gastric cancer.","authors":"Qichen Huang, Junyu Ke, Xinrui Shen, Yitian Xu, Sijun Sun, Chen Huang","doi":"10.1186/s13062-026-00813-4","DOIUrl":"https://doi.org/10.1186/s13062-026-00813-4","url":null,"abstract":"","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147762265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"JUNB transcriptional regulation of KRT20 via ITGB1 activates PI3K/AKT signaling pathway against fibrosis-induced by renal injury.","authors":"Haonan Mei, Xinmiao Ni, Qingyuan Zheng, Hao Tang, Zhiwei Yan, Song Yang, Yufeng Xiong, Yumin Hui, Jun Jian, Jingsong Wang, Xiangxiang Yang, Xiuheng Liu, Zhiyuan Chen","doi":"10.1186/s13062-026-00804-5","DOIUrl":"https://doi.org/10.1186/s13062-026-00804-5","url":null,"abstract":"","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147762231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SH3BGRL3 promotes radioresistance and immune evasion in triple-negative breast cancer by regulating Rab27a.","authors":"Li Wang, Fei Lu, Jingyan Gao, Yanli Li, Songqin Li, Man Li, Renyi Dong","doi":"10.1186/s13062-026-00799-z","DOIUrl":"https://doi.org/10.1186/s13062-026-00799-z","url":null,"abstract":"","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147762287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A cyclin D1-CDK4/6-E2F dependency represents an acquired vulnerability in cisplatin-resistant bladder cancer.","authors":"Tsung-Han Hsieh, Han-Pin Kuo, Chun-Hsu Pan, Yu-Chen Lin, Bo-Jyun Lin, Mei-Chuan Chen, Chun-Han Chen","doi":"10.1186/s13062-026-00812-5","DOIUrl":"https://doi.org/10.1186/s13062-026-00812-5","url":null,"abstract":"","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}