title: Necroptosis in acute kidney injury: a shedding light.
abstract: Acute kidney injury (AKI) is a common and severe clinical condition with a heavy healthy burden around the world. In spite of supportive therapies, the mortality associated with AKI remains high. Our limited understanding of the complex cell death mechanism in the process of AKI impedes the development of desirable therapeutics. Necroptosis is a recently identified novel form of cell death contributing to numerable diseases and tissue damages. Increasing evidence has suggested that necroptosis has an important role in the pathogenesis of various types of AKI. Therefore, we present here the signaling pathways and main regulators of necroptosis that are potential candidate for therapeutic strategies. Moreover, we emphasize on the potential role and corresponding mechanisms of necroptosis in AKI based on recent advances, and also discuss the possible therapeutic regimens based on manipulating necroptosis. Taken together, the progress in this field sheds new light into the prevention and management of AKI in clinical practice.
authors.affiliation: Department of Urology, Zhongshan Hospital, Fudan University, Shanghai, China.|Shanghai Key Laboratory of Organ Transplantation, Shanghai, China.
authors.forename: S
authors.initials: S
authors.lastname: Wang
authors.affiliation: Department of Urology, Zhongshan Hospital, Fudan University, Shanghai, China.|Shanghai Key Laboratory of Organ Transplantation, Shanghai, China.
authors.forename: C
authors.identifier: http://orcid.org/0000-0001-9672-0720
authors.initials: C
authors.lastname: Zhang
authors.affiliation: Department of Urology, The First Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: L
authors.initials: L
authors.lastname: Hu
authors.affiliation: Shanghai Key Laboratory of Organ Transplantation, Shanghai, China.|Department of Plastic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
authors.forename: C
authors.initials: C
authors.lastname: Yang
mesh_terms: D058186:Acute Kidney Injury / Q000378:metabolism* / Q000473:pathology* / Q000628:therapy; D000818:Animals; D016923:Cell Death; D006801:Humans; D015398:Signal Transduction