[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-441523-105":59,"doc-detail-441523-en":130},{"code":4,"msg":5,"data":6},0,"success",[7,13,18,23,28,33,38,43,48,51,55],{"id":8,"doc_module":4,"doc_module_name":9,"category_name":10,"show_sort_weight":11,"slug":12},1,"Document","Story & Novel",90,"story-novel",{"id":14,"doc_module":4,"doc_module_name":9,"category_name":15,"show_sort_weight":16,"slug":17},2,"Literature",80,"literature",{"id":19,"doc_module":4,"doc_module_name":9,"category_name":20,"show_sort_weight":21,"slug":22},4,"Exam",70,"exam",{"id":24,"doc_module":4,"doc_module_name":9,"category_name":25,"show_sort_weight":26,"slug":27},5,"Comic",60,"comic",{"id":29,"doc_module":4,"doc_module_name":9,"category_name":30,"show_sort_weight":31,"slug":32},6,"Technology",50,"technology",{"id":34,"doc_module":4,"doc_module_name":9,"category_name":35,"show_sort_weight":36,"slug":37},7,"Healthcare",40,"healthcare",{"id":39,"doc_module":4,"doc_module_name":9,"category_name":40,"show_sort_weight":41,"slug":42},8,"Research & Report",30,"research-report",{"id":44,"doc_module":4,"doc_module_name":9,"category_name":45,"show_sort_weight":46,"slug":47},9,"Religion & Spirituality",20,"religion-spirituality",{"id":46,"doc_module":4,"doc_module_name":9,"category_name":49,"show_sort_weight":46,"slug":50},"World Cup","world-cup",{"id":52,"doc_module":4,"doc_module_name":9,"category_name":53,"show_sort_weight":52,"slug":54},10,"Lifestyle","lifestyle",{"id":56,"doc_module":4,"doc_module_name":9,"category_name":57,"show_sort_weight":24,"slug":58},19,"General","general",{"code":4,"msg":60,"data":61},"ok",{"site_id":62,"language":63,"slug":64,"title":65,"keywords":66,"description":67,"schema_data":68,"social_meta":123,"head_meta":125,"extra_data":127,"updated_unix":129},105,"en","snx16-aggravates-angii-induced-cardiac-hypertrophy-in-mice-via-egfr-transactivation-article-abstract","SNX16 aggravates AngII-induced cardiac hypertrophy in mice via EGFR transactivation - Article Abstract","","Cardiac hypertrophy is a key independent risk factor for heart failure and related cardiovascular deaths worldwide. This study shows that Sorting Nexin 16 (SNX16) is upregulated in hypertrophic hearts and that cardiac-specific SNX16 deletion in male mice markedly suppresses AngII-induced hypertrophy and cardiomyocyte enlargement. AngII stimulation and SNX16 overexpression promote EGFR transactivation and cardiomyocyte growth, largely blocked by the EGFR-pathway inhibitor AZD9291. SNX16 loss also inhibits AngII- or EGF-induced EGFR recycling in endosomal trafficking. Elevated SNX16 and EGFR/Src phosphorylation are confirmed in patient heart tissues, supporting a SNX16-mediated EGFR recycling mechanism.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/snx16-aggravates-angii-induced-cardiac-hypertrophy-in-mice-via-egfr-transactivation-article-abstract/441523/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/snx16-aggravates-angii-induced-cardiac-hypertrophy-in-mice-via-egfr-transactivation-article-abstract/441523.png","ImageObject",300,407,{"name":92,"@type":93},"Damian","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-09-30","2026-09-29",true,{"@type":102,"interactionType":103,"userInteractionCount":14},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What role does SNX16 play in AngII-induced cardiac hypertrophy?","Question",{"text":112,"@type":113},"SNX16 expression is upregulated in hypertrophic hearts, and cardiac-specific deletion of SNX16 significantly inhibits AngII-induced cardiac hypertrophy and cardiomyocyte enlargement.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How does SNX16 influence EGFR signaling in cardiomyocytes?",{"text":117,"@type":113},"AngII stimulation and SNX16 overexpression promote EGFR transactivation, and SNX16 deficiency inhibits AngII- or EGF-induced EGFR recycling during endosomal trafficking.",{"name":119,"@type":110,"acceptedAnswer":120},"What evidence supports SNX16’s mechanism in human disease?",{"text":121,"@type":113},"Heart tissues from patients with cardiac hypertrophy show elevated SNX16 expression along with increased phosphorylation of EGFR and Src, consistent with the proposed mechanism.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},441523,1790757129,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":14,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":41},137451208677,"https://ap-avatar.wpscdn.com/davatar_155a257f0dc6eb9ab79c44ca47cae57d","communications biology Article  \n\n| A Nature Portfolio journal |  | |\n| --- | --- | --- |\n| [https://doi.org/10.1038/s42003-025-09243-w](https://doi.org/10.1038/s42003-025-09243-w) |  |  |\n| SNX16 aggravatesAngII-induced cardiac hypertrophy in mice via EGFR transactivation\u003Cbr> Check for updates |  |  |\n| Lin Xie1,2,3,7, Ke Wen1,4,7, Guan-Hui Yu1,4,7, Xin Li1,2,7, Yu-Ye Zeng1,2, Xu-Hui Qiao2, Bing-Qian Lu1, Lu Chen1, Xiao-leiWang1, Jing He1, Ying-Jiong Lin1, Xiao-Yong Ren1,2, Xin Wu3, Qi-KunYang1,5, Lu-Lu Hu6, YongJi 6, Hong-Bo Xin  1,2,4,8  & Ke-Yu Deng  1,2,4,8  |  |  |\n| Cardiac hypertrophy is an independent risk factor for heart failure (HF) which often leads to cardiovascular disease-related death worldwide. Here we show that the upregulated expressions of Sorting Nexin 16 (SNX16) are evident in the hypertrophic hearts. Cardiac-specific deletion of SNX16 significantly inhibited AngII-induced cardiac hypertrophy and cardiomyocytic enlargement in male mice. In addition, we observed that both AngII stimulation and SNX16 overexpression markedly enlarged cardiomyocytes and promoted EGFR transactivation, and these effects were almost completely abolished by AZD9291, an inhibitor of the EGFR pathway. SNX16 deficiency significantly inhibitedAngII-orEGF-induced recycling of EGFR in endosomaltrafficking in cardiomyocytes. Finally, the elevated expression of SNX16 and the phosphorylation of EGFR and Src were further confirmed in heart tissues from patients with cardiac hypertrophy. Therefore, the present study demonstrates that SNX16-mediated transactivation of EGFR plays a key role in AngII-induced cardiac hypertrophy via enhancing the recycling of EGFR. |  |  |\n| Cardiac hypertrophy is an independent risk factor for many serious cardiovascular events1, including heart failure (HF), which is one of the leading causes of cardiovascular disease-related death worldwide2. Angiotensin II (AngII), a well-known hypertrophic stimulus, promotes the expression of hypertrophic genes such as Nppa and Nppb in cardiomyocytes, leading to cardiac hypertrophy and heart remodeling3. Transactivation of epidermal growth factor receptor (EGFR, a receptor tyrosine kinase) mediated by AngII, is considered to play a central role in cardiac hypertrophy. AngII activates EGFR transactivation through the metalloprotease ADAM17-mediated proHB-EGF shedding, in which AngII binds to its G proteincoupled receptor AT1R(AngII type1receptor)to activate ADAM17via Srcmediated intracellular Ca2+/ROS and subsequently leads to EGFR transactivation and activation of downstream signaling pathways, including the Ras/ERK1/2 and Ras/PI3K/Akt/mTOR/S6 kinases, to modulate cellular growth and proliferation4. However, the underlying mechanism of EGFR transactivation in cardiac hypertrophy is still not fully understood.\u003Cbr>Sorting nexins (SNXs) are a family of proteins containing phoxhomology(PX)domains that are conserved from yeast to mammals, and34 | mammalian family members have been identified5,6. SNXs play critical roles in endocytic trafficking, including endocytosis, endosomal sorting and endosomal signaling, since the PX domain binds to phosphatidylinostil-3-monophosphates (PI3Ps), which are mostly enriched in endosomes7. More importantly, numerous studies have reported that dysfunction of sorting nexins is increasingly associated with many diseases, such as Alzheimer’s disease, carcinomas, hypertension and pathogenic infection6,8.\u003Cbr>Sorting nexin 16 (SNX16), a member of the SNX family, contains 343 amino acids containing a PX domain, a coiled-coil (CC) domain and a C-terminal region. The PX domain is associated with membranes via interactions with PI3P in endosomes, and homo-oligomerization and higher-order assembly occur via the CC domain9–11. Studies have indicated that SNX16 is distributed in all three different endosomes, including early endosomes9, 12–14, recycling endosomes12, 15, and late endosomes9, 13, 15, and participates in intracellular protein sorting, such as traffick","cbCair89QQAD102M","https://ap.wps.com/l/cbCair89QQAD102M","pdf",8517782,12,"English","# Background\n## Cardiac hypertrophy and AngII signaling\n## EGFR transactivation and downstream pathways\n# Role of Sorting Nexins\n## PX-domain endosomal trafficking\n## SNX16 structure and disease associations\n# Study Aim and Findings\n## SNX16 upregulation in hypertrophic hearts\n## Effects of cardiac-specific SNX16 deletion\n## Effects of SNX16 overexpression\n## EGFR transactivation, recycling, and inhibition by AZD9291\n## Confirmation in human patient tissues","[{\"question\":\"What role does SNX16 play in AngII-induced cardiac hypertrophy?\",\"answer\":\"SNX16 expression is upregulated in hypertrophic hearts, and cardiac-specific deletion of SNX16 significantly inhibits AngII-induced cardiac hypertrophy and cardiomyocyte enlargement.\"},{\"question\":\"How does SNX16 influence EGFR signaling in cardiomyocytes?\",\"answer\":\"AngII stimulation and SNX16 overexpression promote EGFR transactivation, and SNX16 deficiency inhibits AngII- or EGF-induced EGFR recycling during endosomal trafficking.\"},{\"question\":\"What evidence supports SNX16’s mechanism in human disease?\",\"answer\":\"Heart tissues from patients with cardiac hypertrophy show elevated SNX16 expression along with increased phosphorylation of EGFR and Src, consistent with the proposed mechanism.\"}]","SNX16 aggravates AngII-induced cardiac hypertrophy in mice via EGFR transactivation - Article Abstract | PDF",1790696408]