{"title":"内皮细胞坏死导致溶血和微血管病变","authors":"Gregory B. Lim","doi":"10.1038/s41569-025-01185-4","DOIUrl":null,"url":null,"abstract":"Endothelial cells in ischaemic microvessels undergo necroptosis, which is linked to haemolysis and the deposition of haemolysed red blood cell membranes at the sites of endothelial cell death. This process might be a haemostatic mechanism to prevent interstitial bleeding; however, excessive aggregation can cause microvascular obstruction and microangiopathy.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"245 1","pages":""},"PeriodicalIF":41.7000,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Endothelial cell necroptosis induces haemolysis and microangiopathy\",\"authors\":\"Gregory B. Lim\",\"doi\":\"10.1038/s41569-025-01185-4\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Endothelial cells in ischaemic microvessels undergo necroptosis, which is linked to haemolysis and the deposition of haemolysed red blood cell membranes at the sites of endothelial cell death. This process might be a haemostatic mechanism to prevent interstitial bleeding; however, excessive aggregation can cause microvascular obstruction and microangiopathy.\",\"PeriodicalId\":18976,\"journal\":{\"name\":\"Nature Reviews Cardiology\",\"volume\":\"245 1\",\"pages\":\"\"},\"PeriodicalIF\":41.7000,\"publicationDate\":\"2025-06-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nature Reviews Cardiology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1038/s41569-025-01185-4\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature Reviews Cardiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41569-025-01185-4","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
Endothelial cell necroptosis induces haemolysis and microangiopathy
Endothelial cells in ischaemic microvessels undergo necroptosis, which is linked to haemolysis and the deposition of haemolysed red blood cell membranes at the sites of endothelial cell death. This process might be a haemostatic mechanism to prevent interstitial bleeding; however, excessive aggregation can cause microvascular obstruction and microangiopathy.
期刊介绍:
Nature Reviews Cardiology aims to be the go-to source for reviews and commentaries in the scientific and clinical communities it serves. Focused on providing authoritative and accessible articles enriched with clear figures and tables, the journal strives to offer unparalleled service to authors, referees, and readers, maximizing the usefulness and impact of each publication. It covers a broad range of content types, including Research Highlights, Comments, News & Views, Reviews, Consensus Statements, and Perspectives, catering to practising cardiologists and cardiovascular research scientists. Authored by renowned clinicians, academics, and researchers, the content targets readers in the biological and medical sciences, ensuring accessibility across various disciplines. In-depth Reviews offer up-to-date information, while Consensus Statements provide evidence-based recommendations. Perspectives and News & Views present topical discussions and opinions, and the Research Highlights section filters primary research from cardiovascular and general medical journals. As part of the Nature Reviews portfolio, Nature Reviews Cardiology maintains high standards and a wide reach.