RIPK1 in necroptosis and recent progress in related pharmaceutics

Necroptosis is a programmed form of cell death. Receptor-interacting serine/threonine protein kinase l (RIPK1) is a crucial protein kinase that regulates the necroptosis pathway. Increased expression of death receptor family ligands such as tumor necrosis factor (TNF) increases the susceptibility of...

Full description

Saved in:
Bibliographic Details
Main Authors: Kunhou Yao, Zhihao Shi, Fengya Zhao, Cong Tan, Yixin Zhang, Hao Fan, Yingzhe Wang, Xingwang Li, Jun Kong, Qun Wang, Dingxi Li
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-02-01
Series:Frontiers in Immunology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2025.1480027/full
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1823859430696943616
author Kunhou Yao
Zhihao Shi
Fengya Zhao
Cong Tan
Yixin Zhang
Hao Fan
Yingzhe Wang
Xingwang Li
Jun Kong
Qun Wang
Dingxi Li
author_facet Kunhou Yao
Zhihao Shi
Fengya Zhao
Cong Tan
Yixin Zhang
Hao Fan
Yingzhe Wang
Xingwang Li
Jun Kong
Qun Wang
Dingxi Li
author_sort Kunhou Yao
collection DOAJ
description Necroptosis is a programmed form of cell death. Receptor-interacting serine/threonine protein kinase l (RIPK1) is a crucial protein kinase that regulates the necroptosis pathway. Increased expression of death receptor family ligands such as tumor necrosis factor (TNF) increases the susceptibility of cells to apoptosis and necroptosis. RIPK1, RIPK3, and mixed-lineage kinase-like domain (MLKL) proteins mediate necrosis. RIPK1-mediated necroptosis further promotes cell death and inflammation in the pathogenesis of liver injury, skin diseases, and neurodegenerative diseases. The N-terminal kinase domain of RIPK1 is significant in the induction of cell death and can be used as a vital drug target for inhibitors. In this paper, we outline the pathways of necroptosis and the role RIPK1 plays in them and suggest that targeting RIPK1 in therapy may help to inhibit multiple cell death pathways.
format Article
id doaj-art-d8f265dbd1044b529c4460932c6889db
institution Kabale University
issn 1664-3224
language English
publishDate 2025-02-01
publisher Frontiers Media S.A.
record_format Article
series Frontiers in Immunology
spelling doaj-art-d8f265dbd1044b529c4460932c6889db2025-02-11T05:10:24ZengFrontiers Media S.A.Frontiers in Immunology1664-32242025-02-011610.3389/fimmu.2025.14800271480027RIPK1 in necroptosis and recent progress in related pharmaceuticsKunhou Yao0Zhihao Shi1Fengya Zhao2Cong Tan3Yixin Zhang4Hao Fan5Yingzhe Wang6Xingwang Li7Jun Kong8Qun Wang9Dingxi Li10Department of General Surgery, Huaihe Hospital of Henan University, Kaifeng, ChinaSchool of Basic Medicine, Henan University, Kaifeng, ChinaSchool of Basic Medicine, Henan University, Kaifeng, ChinaSchool of Basic Medicine, Henan University, Kaifeng, ChinaSchool of Basic Medicine, Henan University, Kaifeng, ChinaSchool of Basic Medicine, Henan University, Kaifeng, ChinaSchool of Basic Medicine, Henan University, Kaifeng, ChinaDepartment of General Surgery, Huaihe Hospital of Henan University, Kaifeng, ChinaSchool of Basic Medicine, Henan University, Kaifeng, ChinaSchool of Basic Medicine, Henan University, Kaifeng, ChinaDepartment of Gynaecology, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, ChinaNecroptosis is a programmed form of cell death. Receptor-interacting serine/threonine protein kinase l (RIPK1) is a crucial protein kinase that regulates the necroptosis pathway. Increased expression of death receptor family ligands such as tumor necrosis factor (TNF) increases the susceptibility of cells to apoptosis and necroptosis. RIPK1, RIPK3, and mixed-lineage kinase-like domain (MLKL) proteins mediate necrosis. RIPK1-mediated necroptosis further promotes cell death and inflammation in the pathogenesis of liver injury, skin diseases, and neurodegenerative diseases. The N-terminal kinase domain of RIPK1 is significant in the induction of cell death and can be used as a vital drug target for inhibitors. In this paper, we outline the pathways of necroptosis and the role RIPK1 plays in them and suggest that targeting RIPK1 in therapy may help to inhibit multiple cell death pathways.https://www.frontiersin.org/articles/10.3389/fimmu.2025.1480027/fullRIPK1necroptosisprogrammed cell deathinflammationkinase domainpharmaceutics
spellingShingle Kunhou Yao
Zhihao Shi
Fengya Zhao
Cong Tan
Yixin Zhang
Hao Fan
Yingzhe Wang
Xingwang Li
Jun Kong
Qun Wang
Dingxi Li
RIPK1 in necroptosis and recent progress in related pharmaceutics
Frontiers in Immunology
RIPK1
necroptosis
programmed cell death
inflammation
kinase domain
pharmaceutics
title RIPK1 in necroptosis and recent progress in related pharmaceutics
title_full RIPK1 in necroptosis and recent progress in related pharmaceutics
title_fullStr RIPK1 in necroptosis and recent progress in related pharmaceutics
title_full_unstemmed RIPK1 in necroptosis and recent progress in related pharmaceutics
title_short RIPK1 in necroptosis and recent progress in related pharmaceutics
title_sort ripk1 in necroptosis and recent progress in related pharmaceutics
topic RIPK1
necroptosis
programmed cell death
inflammation
kinase domain
pharmaceutics
url https://www.frontiersin.org/articles/10.3389/fimmu.2025.1480027/full
work_keys_str_mv AT kunhouyao ripk1innecroptosisandrecentprogressinrelatedpharmaceutics
AT zhihaoshi ripk1innecroptosisandrecentprogressinrelatedpharmaceutics
AT fengyazhao ripk1innecroptosisandrecentprogressinrelatedpharmaceutics
AT congtan ripk1innecroptosisandrecentprogressinrelatedpharmaceutics
AT yixinzhang ripk1innecroptosisandrecentprogressinrelatedpharmaceutics
AT haofan ripk1innecroptosisandrecentprogressinrelatedpharmaceutics
AT yingzhewang ripk1innecroptosisandrecentprogressinrelatedpharmaceutics
AT xingwangli ripk1innecroptosisandrecentprogressinrelatedpharmaceutics
AT junkong ripk1innecroptosisandrecentprogressinrelatedpharmaceutics
AT qunwang ripk1innecroptosisandrecentprogressinrelatedpharmaceutics
AT dingxili ripk1innecroptosisandrecentprogressinrelatedpharmaceutics