{"title":"From symbiosis to immunity: the evolutionary revival of mitochondrial defense programs in inflammatory diseases.","authors":"Weilong Hong, Shiyun Long, Milad Ashrafizadeh, Gautam Sethi, Chenyang Duan","doi":"10.1186/s12964-026-02736-z","DOIUrl":"https://doi.org/10.1186/s12964-026-02736-z","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147349516","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}
Pub Date : 2026-03-04DOI: 10.1186/s12964-026-02777-4
Mingjie Jiang, Yongchao Yu, Zan Jiao, Tong Wu, Kang Ning, Zhongyuan Yang, Weichao Chen, Ankui Yang
{"title":"Dying cells as architects of the stem cell niche: a conserved mechanism driving tissue regeneration and tumor therapy resistance.","authors":"Mingjie Jiang, Yongchao Yu, Zan Jiao, Tong Wu, Kang Ning, Zhongyuan Yang, Weichao Chen, Ankui Yang","doi":"10.1186/s12964-026-02777-4","DOIUrl":"https://doi.org/10.1186/s12964-026-02777-4","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147357628","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}
Pub Date : 2026-03-03DOI: 10.1186/s12964-026-02762-x
Romina Cabrera-Rodríguez, Anna Pons-Grifols, María Pernas, Concepción Casado, Rodrigo Trujillo-González, Iria Lorenzo-Sánchez, Iriome Reyes-Castañeda, Benjamin Trinité, Julià Blanco, Agustin Valenzuela-Fernández
{"title":"TARDBP as a regulator of HIV-1 assembly and infection: a review of targeting the viral capsid precursor Pr55Gag and limiting viral core entry.","authors":"Romina Cabrera-Rodríguez, Anna Pons-Grifols, María Pernas, Concepción Casado, Rodrigo Trujillo-González, Iria Lorenzo-Sánchez, Iriome Reyes-Castañeda, Benjamin Trinité, Julià Blanco, Agustin Valenzuela-Fernández","doi":"10.1186/s12964-026-02762-x","DOIUrl":"https://doi.org/10.1186/s12964-026-02762-x","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147345646","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}
Pub Date : 2026-03-03DOI: 10.1186/s12964-026-02771-w
Nikolina Stojanović, Anja Rac, Marija Lončarić, Ana Tadijan, Mladen Paradžik, Marta Acman, Jonathan D Humphries, Martin J Humphries, Andreja Ambriović-Ristov
{"title":"KANK2 at focal adhesions regulates their maintenance and dynamics, while at fibrillar adhesions it influences cell migration via microtubule-dependent mechanism.","authors":"Nikolina Stojanović, Anja Rac, Marija Lončarić, Ana Tadijan, Mladen Paradžik, Marta Acman, Jonathan D Humphries, Martin J Humphries, Andreja Ambriović-Ristov","doi":"10.1186/s12964-026-02771-w","DOIUrl":"https://doi.org/10.1186/s12964-026-02771-w","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147349487","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}
Pub Date : 2026-03-03DOI: 10.1186/s12964-026-02764-9
Jolene Wei Ling Lee, Adeline Su Lyn Ng, Eng-King Tan, Li Zeng
{"title":"NOTCH3 Mutations in CADASIL: a multicellular perspective on neurodegeneration.","authors":"Jolene Wei Ling Lee, Adeline Su Lyn Ng, Eng-King Tan, Li Zeng","doi":"10.1186/s12964-026-02764-9","DOIUrl":"https://doi.org/10.1186/s12964-026-02764-9","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147349496","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}
Background: Pathological cardiac hypertrophy frequently leads to heart failure (HF). UBA1, the key E1 ubiquitin-activating enzyme, initiates ubiquitin-proteasome signaling and contributes to various diseases, yet its mechanism in cardiac hypertrophy remains unclear.
Methods: Cardiac hypertrophy model was induced by either Ang II stimulation or TAC in vitro and in vivo. Mice received rAAV9-UBA1-siRNA or rAAV9-UBA1 for UBA1 knockdown or overexpression, respectively.
Results: We found UBA1 upregulated in murine and human hypertrophic hearts. Cardiomyocyte-specific UBA1 knockdown protected against TAC-induced hypertrophy, fibrosis, oxidative stress, and dysfunction, with downregulation of ATG5 and autophagy induction, whereas myocardial UBA1 overexpression exacerbated these effects. Mechanistically, UBA1 directly interacted with ATG5 and promoted its ubiquitination for degradation, leading to autophagy inactivation and hypertrophy. Furthermore, ATG5 deletion abrogated the protection of UBA1 knockdown against cardiomyocyte hypertrophy.
Conclusions: UBA1 regulates cardiac hypertrophy through suppression of ATG5-mediated autophagy and propose UBA1 as a therapeutic target for hypertrophic cardiomyopathy.
{"title":"UBA1 promotes cardiac hypertrophy by suppressing autophagy via targeting ATG5 for ubiquitination.","authors":"Qiu-Yue Lin, Wei-Jia Yu, Jia-Xin Li, Wen-Xi Jiang, Shu-Jing Liu, Hai-Lian Bi, Hui-Hua Li","doi":"10.1186/s12964-026-02761-y","DOIUrl":"https://doi.org/10.1186/s12964-026-02761-y","url":null,"abstract":"<p><strong>Background: </strong>Pathological cardiac hypertrophy frequently leads to heart failure (HF). UBA1, the key E1 ubiquitin-activating enzyme, initiates ubiquitin-proteasome signaling and contributes to various diseases, yet its mechanism in cardiac hypertrophy remains unclear.</p><p><strong>Methods: </strong>Cardiac hypertrophy model was induced by either Ang II stimulation or TAC in vitro and in vivo. Mice received rAAV9-UBA1-siRNA or rAAV9-UBA1 for UBA1 knockdown or overexpression, respectively.</p><p><strong>Results: </strong>We found UBA1 upregulated in murine and human hypertrophic hearts. Cardiomyocyte-specific UBA1 knockdown protected against TAC-induced hypertrophy, fibrosis, oxidative stress, and dysfunction, with downregulation of ATG5 and autophagy induction, whereas myocardial UBA1 overexpression exacerbated these effects. Mechanistically, UBA1 directly interacted with ATG5 and promoted its ubiquitination for degradation, leading to autophagy inactivation and hypertrophy. Furthermore, ATG5 deletion abrogated the protection of UBA1 knockdown against cardiomyocyte hypertrophy.</p><p><strong>Conclusions: </strong>UBA1 regulates cardiac hypertrophy through suppression of ATG5-mediated autophagy and propose UBA1 as a therapeutic target for hypertrophic cardiomyopathy.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328252","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}
Pub Date : 2026-02-27DOI: 10.1186/s12964-026-02731-4
Jingyu Dai, Yibing Liu, Tao Tang, Mingsheng Tang, Jun Chen, Hailan Wang, Xi Liu
{"title":"Apoptotic vesicles in cancer: research progress in physiology and therapy.","authors":"Jingyu Dai, Yibing Liu, Tao Tang, Mingsheng Tang, Jun Chen, Hailan Wang, Xi Liu","doi":"10.1186/s12964-026-02731-4","DOIUrl":"https://doi.org/10.1186/s12964-026-02731-4","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147312735","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}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号