RIP3: a molecular switch for necrosis and inflammation.
TLDR
The current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases is reviewed.Abstract:
The receptor-interacting protein kinase 3 (RIP3/RIPK3) has emerged as a critical regulator of programmed necrosis/ necroptosis, an inflammatory form of cell death with important functions in pathogen-induced and sterile inflammation. RIP3 activation is tightly regulated by phosphorylation, ubiquitination, and caspase-mediated cleavage. These post-translational modifications coordinately regulate the assembly of a macromolecular signaling complex termed the necrosome. Recently, several reports indicate that RIP3 can promote inflammation independent of its pronecrotic activity. Here, we review our current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases.read more
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Endothelin-1 axes in the framework of predictive, preventive and personalised (3P) medicine.
Adriana Torres Crigna,Barbara Link,Marek Samec,Frank A. Giordano,Peter Kubatka,Olga Golubnitschaja +5 more
TL;DR: In this article, an in-depth analysis of the involvement of ET-1 and related regulatory pathways in physiological and pathophysiological processes and estimates its capacity as a predictor of ageing and related pathologies, a sensor of lifestyle quality and progression of suboptimal health conditions to diseases for their targeted prevention and as a potent target for cost-effective treatments tailored to the person.
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Natural Compounds As Modulators of Non-apoptotic Cell Death in Cancer Cells.
TL;DR: The role of natural compounds from plants, microorganisms and sea life forms, which are able to induce non-apoptotic cell death in tumor cells, namely autophagy and necroptosis are underlined.
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RIPK3-mediated inflammation is a conserved β cell response to ER stress.
Bingyuan Yang,Lisette A. Maddison,Karolina E. Zaborska,Chunhua Dai,Linlin Yin,Zihan Tang,Liqing Zang,Liqing Zang,David A. Jacobson,Alvin C. Powers,Alvin C. Powers,Wenbiao Chen +11 more
TL;DR: RIPK3-mediated induction of proinflammatory mediators is a conserved, previously unrecognized β cell response to metabolic stress and a mediator of the ensuing islet inflammation.
Journal ArticleDOI
Tubular epithelial cells in renal clear cell carcinoma express high RIPK1/3 and show increased susceptibility to TNF receptor 1-induced necroptosis
Rafia S. Al-Lamki,Wanhua Lu,P Manalo,Jun Wang,Anne Y. Warren,Aviva M. Tolkovsky,Jordan S. Pober,John Bradley +7 more
TL;DR: It is concluded that most high-grade RCC cells express increased amounts of RIPK1 and RIPK3 and are poised to undergo necroptosis in response to TNFR1 signaling, implying that different subsets of cells respond differently to TNF-α.
Journal ArticleDOI
Mechanisms of Regulated Cell Death: Current Perspectives.
Sara F Santagostino,Charles-Antoine Assenmacher,James C. Tarrant,Adeyemi O Adedeji,Enrico Radaelli +4 more
TL;DR: In this article, the current understanding of the molecular machinery of each type of non-apoptotic RCD mechanisms is outlined Due to the continuous discovery of new mechanisms or nuances of previously described processes, the limitations of the terms apoptosis and necrosis to indicate microscopic findings are also reported In addition, the need for a standard panel of biomarkers and functional tests to adequately characterize the underlying RCD and its role as a mechanism of disease is considered
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