{"title":"贝利斯-斯特林奖讲座：KATP通道病理生理学-全身奥德赛。","authors":"Colin G. Nichols","doi":"10.1113/JP287415","DOIUrl":null,"url":null,"abstract":"<p>First identified 40 years ago in cardiac myocytes, ATP-sensitive potassium (K<sub>ATP</sub>) channels have been found in almost all excitable tissues, with paradigmatic inhibition by ATP and activation by ADP underlying their physiological role in coupling cellular metabolism to electrical activity. Cloning of the underlying genes, 30 years ago, revealed their unique assembly as four Kir6.x pore-forming subunit proteins and four sulfonylurea receptor (SURx) subunit proteins and has since led to discovery of a spectrum of monogenic diseases resulting from gain- (GOF) or loss-of-function (LOF) mutations, in turn leading to recognition of novel physiological roles and pathophysiological consequences throughout the body. With this perspective, this lecture represents a personal view of these discoveries and the potential for future pathophysiological insights.\n\n <figure>\n <div><picture>\n <source></source></picture><p></p>\n </div>\n </figure></p>","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":"603 11","pages":"3293-3305"},"PeriodicalIF":4.7000,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Bayliss–Starling Prize Lecture: KATP channel pathophysiology – a whole-body odyssey\",\"authors\":\"Colin G. Nichols\",\"doi\":\"10.1113/JP287415\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>First identified 40 years ago in cardiac myocytes, ATP-sensitive potassium (K<sub>ATP</sub>) channels have been found in almost all excitable tissues, with paradigmatic inhibition by ATP and activation by ADP underlying their physiological role in coupling cellular metabolism to electrical activity. Cloning of the underlying genes, 30 years ago, revealed their unique assembly as four Kir6.x pore-forming subunit proteins and four sulfonylurea receptor (SURx) subunit proteins and has since led to discovery of a spectrum of monogenic diseases resulting from gain- (GOF) or loss-of-function (LOF) mutations, in turn leading to recognition of novel physiological roles and pathophysiological consequences throughout the body. With this perspective, this lecture represents a personal view of these discoveries and the potential for future pathophysiological insights.\\n\\n <figure>\\n <div><picture>\\n <source></source></picture><p></p>\\n </div>\\n </figure></p>\",\"PeriodicalId\":50088,\"journal\":{\"name\":\"Journal of Physiology-London\",\"volume\":\"603 11\",\"pages\":\"3293-3305\"},\"PeriodicalIF\":4.7000,\"publicationDate\":\"2025-05-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Physiology-London\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1113/JP287415\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Physiology-London","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1113/JP287415","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
Bayliss–Starling Prize Lecture: KATP channel pathophysiology – a whole-body odyssey
First identified 40 years ago in cardiac myocytes, ATP-sensitive potassium (KATP) channels have been found in almost all excitable tissues, with paradigmatic inhibition by ATP and activation by ADP underlying their physiological role in coupling cellular metabolism to electrical activity. Cloning of the underlying genes, 30 years ago, revealed their unique assembly as four Kir6.x pore-forming subunit proteins and four sulfonylurea receptor (SURx) subunit proteins and has since led to discovery of a spectrum of monogenic diseases resulting from gain- (GOF) or loss-of-function (LOF) mutations, in turn leading to recognition of novel physiological roles and pathophysiological consequences throughout the body. With this perspective, this lecture represents a personal view of these discoveries and the potential for future pathophysiological insights.
期刊介绍：
The Journal of Physiology publishes full-length original Research Papers and Techniques for Physiology, which are short papers aimed at disseminating new techniques for physiological research. Articles solicited by the Editorial Board include Perspectives, Symposium Reports and Topical Reviews, which highlight areas of special physiological interest. CrossTalk articles are short editorial-style invited articles framing a debate between experts in the field on controversial topics. Letters to the Editor and Journal Club articles are also published. All categories of papers are subjected to peer reivew.
The Journal of Physiology welcomes submitted research papers in all areas of physiology. Authors should present original work that illustrates new physiological principles or mechanisms. Papers on work at the molecular level, at the level of the cell membrane, single cells, tissues or organs and on systems physiology are all acceptable. Theoretical papers and papers that use computational models to further our understanding of physiological processes will be considered if based on experimentally derived data and if the hypothesis advanced is directly amenable to experimental testing. While emphasis is on human and mammalian physiology, work on lower vertebrate or invertebrate preparations may be suitable if it furthers the understanding of the functioning of other organisms including mammals.
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