The role of necroptosis in disease and treatment

Liu, Huan; Xie, Xin; Ren, Yuanyuan; Shao, Zhaogang; Zhang, Nie; Li, Liantao; Ding, Xin; Zhang, Longzhen

doi:10.1002/mco2.108

Cited by 50 publications

(38 citation statements)

References 220 publications

(246 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Intracellular ROS accumulation can induce cell necroptosis, which is a new type of programmed cell death with the characteristics of both apoptosis and necrosis. Necroptosis plays an important role in maintaining cell homeostasis, regulating tumor immunity and inflammatory response, and mediating ischemic injury and several other pathophysiological processes [ 49 , 50 ]. As two important mediators of necroptosis, RIPK1 combines with RIPK3 to form necrosomes and phosphorylate MLKL, which then transfers to cell membrane and ruptures it, and exaggerates cell necroptosis finally [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Suppresses Skin Fibroblast Proliferation via Oxidative Stress Alleviation and Necroptosis Inhibition

Zhu

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Keloid is a common dermatofibrotic disease with excessive skin fibroblast proliferation. Hydrogen sulfide (H2S) as the third gasotransmitter improves fibrosis of various organs and tissues. Our study is aimed at investigating the effects and possible mechanisms of H2S on skin fibroblast proliferation. Scar tissues from six patients with keloid and discarded skin tissue from six normal control patients were collected after surgery, respectively. Plasma H2S content and skin H2S production in patients with keloid were measured. Keloid fibroblasts and transforming growth factor-β1- (TGF-β1, 10 ng/mL) stimulated normal skin fibroblasts were pretreated with H2S donor as NaHS (50 μM) for 4 h. Cell migration after scratch was assessed. The expressions of α-smooth muscle actin (α-SMA), proliferating cell nuclear antigen (PCNA), collagen I, and collagen III were detected by immunofluorescence, real-time PCR, and/or Western blot. Intracellular superoxide anion and mitochondrial superoxide were evaluated by dihydroethidium (DHE) and MitoSOX staining, respectively. Mitochondrial membrane potential was detected by JC-1 staining. Apoptotic cells were detected by TDT-mediated dUTP nick end labeling (TUNEL). The expressions of receptor interacting protein kinase 1 (RIPK1), RIPK3, and mixed lineage kinase domain-like protein (MLKL) were measured by Western blot. We found that H2S production was impaired in both the plasma and skin of patients with keloid. In keloid fibroblasts and TGF-β1-stimulated normal skin fibroblasts, exogenous H2S supplementation suppressed the expressions of α-SMA, PCNA, collagen I, and collagen III, reduced intracellular superoxide anion and mitochondrial superoxide, improved the mitochondrial membrane potential, decreased the positive rate of TUNEL staining, and inhibited RIPK1 and RIPK3 expression as well as MLKL phosphorylation. Overall, H2S suppressed skin fibroblast proliferation via oxidative stress alleviation and necroptosis inhibition.

show abstract

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Suppresses Skin Fibroblast Proliferation via Oxidative Stress Alleviation and Necroptosis Inhibition

Zhu

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…In 2018, such a type of programmed necrosis, not dependent on the activation of cysteine-aspartic proteases (caspases), and mainly governed by RIP1, receptor-interacting serine/threonine protein kinase 3 (RIP3) and substrate mixed lineage kinase domain like pseudokinase (MLKL) was called NEC [ 23 ]. NEC controls cell homeostasis, neurodegeneration, infectious diseases, inflammation, cardiovascular and skin diseases, acute kidney injury, and cancer [ 24 ].…”

Section: Apoptosis and Necroptosis: Overview On Molecular Mechanismsmentioning

confidence: 99%

Necroptosis and Prostate Cancer: Molecular Mechanisms and Therapeutic Potential

Beretta

Zaffaroni

2022

Cells

View full text Add to dashboard Cite

Necroptosis is a programmed form of necrosis characterized by mitochondrial alterations and plasma membrane permeabilization resulting in the release of cytoplasmic content into extracellular space, and leading to inflammatory reactions. Besides its critical role in viral defense mechanisms and inflammatory diseases, necroptosis plays pivotal functions in the drug response of tumors, including prostate cancer. Necroptosis is mainly governed by kinase enzymes, including RIP1, RIP3, and MLKL, and conversely to apoptosis, is a caspase-independent mechanism of cell death. Numerous compounds induce necroptosis in prostate cancer models, including (i) compounds of natural origin, (ii) synthetic and semisynthetic small molecules, and (iii) selenium and selenium-based nanoparticles. Here, we overview the molecular mechanisms underlying necroptosis and discuss the possible implications of drugs inducing necroptosis for prostate cancer therapy.

show abstract

“…Necroptosis, a special type of cell death is triggered by a series of death receptors such as tumor necrosis factor receptor 1 (TNFR1), TNFR2 and Fas (for review see [5]). Morphology of cell undergoing necroptosis is similar to that of necrosis.…”

Section: Necrosis and Necroptosis And Regulation By Calcium Transportmentioning

confidence: 99%

“…Necrosis is considered to be an uncontrolled cell death that results in disruption of membrane integrity and causes an inflammatory response [4]. Necroptosis is a programmed version of necrosis [5]. Autophagy as another programmed cell death is an evolutionarily conserved degradation pathway, where over 40 autophagyrelated genes/proteins are involved [6].…”

mentioning

confidence: 99%

Involvement of calcium signaling in different types of cell death in cancer

Babula¹,

Križanová²

2022

neo

View full text Add to dashboard Cite

Programmed cell death is a basic feature of chemotherapeutic (and also radiotherapeutic) intervention.Induction of cell death in tumor cells aims to kill preferentially the tumor cells, with minimal impact on the normal cells. Although apoptosis is the most obvious type of cell death induced by chemotherapeutics, several other types can also be activated, especially in conditions, where cells are resistant to apoptosis induction. Calcium signaling was shown to play an indisputable role in the activation of different types of cell death. Local increase of the calcium in time and precise place of this increase is secured by calcium transport systems. In this review, we summarized the involvement of some calcium transport systems in apoptosis, autophagy, necroptosis, ferroptosis, and mitophagy during cancer development and treatment.

show abstract

The role of necroptosis in disease and treatment

Cited by 50 publications

References 220 publications

Hydrogen Sulfide Suppresses Skin Fibroblast Proliferation via Oxidative Stress Alleviation and Necroptosis Inhibition

Hydrogen Sulfide Suppresses Skin Fibroblast Proliferation via Oxidative Stress Alleviation and Necroptosis Inhibition

Necroptosis and Prostate Cancer: Molecular Mechanisms and Therapeutic Potential

Involvement of calcium signaling in different types of cell death in cancer

Contact Info

Product

Resources

About