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      Necrostatin-1 and necroptosis inhibition: Pathophysiology and therapeutic implications

      review-article
      Author(s): , *
      Publication date (Electronic):
      Journal: Pharmacological Research
      Publisher: Elsevier Ltd.
      Keywords: AAA, abdominal aortic aneurysm, AD, Alzheimer’s disease, AKI, acute kidney injury, ALI, acute lung injury, ALS, amyotrophic lateral sclerosis, AMD, age-related macular degeneration, CaMKII, Ca2+/calmodulin-dependent protein kinase II, cIAP1/2, cellular inhibitor of apoptosis proteins 1 and 2, COVID-19, coronavirus disease 2019, Cyp-D, cyclophilin-D, DAMPs, damage-associated molecular patterns, ERS, endoplasmic reticulum stress, FADD, fas associated via death domain, FHF, fulminant hepatic failure, GSH, glutathione, HD, Huntington’s disease, HG, high glucose, HI, hypoxia-ischemia, HIV-1, human immunodeficiency virus type 1, HMGB1, high mobility group box 1, I/R, Ischemia-reperfusion, ICH, intracerebral hemorrhage, IDO, indoleamine 2,3-dioxygenase, IL, interleukin, LDL, low density lipoprotein, LMP, lysosomal membrane permeabilization, LPS, lipopolysaccharide, MI, myocardial infarction, MLKL, mixed lineage kinase domain-like protein, MPTP, mitochondrial permeability transition pore, MTH-Trp, methyl-thiohydantoin-tryptophan, mTOR, mechanistic target of rapamycin, Nec-1, Necrostatin-1, Nec-1i, Necrostatin-1 inactive, Nec-1s, Necrostatin-1 stable, NF-κB, nuclear factor kappa B, ox-LDL, oxidized LDL, PARP1, polymerase 1, PCD, programmed cell death, PD, Parkinson’s disease, PRR, pattern recognition receptor, PYGL, glycogen phosphorylase, RDA, RIP1-dependent apoptosis, RGAG, advanced glycation end products, RGCs, retinal ganglion cells, RIA, RIP1-indipendent apoptosis, RIP1, receptor interacting protein 1, RIP3, receptor interacting protein 3, ROS, reactive oxygen species, RPE, retinal pigment epithelial, SAH, subarachnoid Hemorrhage, SCI, spinal cord injury, SIRS, systemic inflammatory response syndrome, TBI, traumatic brain injury, TNF, tumor necrosis factor, TNFR1, TNF receptor 1, TRADD, TNFR-associated death domain, TRAF2, TNFR-associated factor 2, necrostatin-1, Necroptosis, Disease models, Anti-Inflammation, COVID-19

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          Abstract

          Necrostatin-1 (Nec-1) is a RIP1-targeted inhibitor of necroptosis, a form of programmed cell death discovered and investigated in recent years. There are already many studies demonstrating the essential role of necroptosis in various diseases, including inflammatory diseases, cardiovascular diseases and neurological diseases. However, the potential of Nec-1 in diseases has not received much attention. Nec-1 is able to inhibit necroptosis signaling pathway and thus ameliorate necroptotic cell death in disease development. Recent research findings indicate that Nec-1 could be applied in several types of diseases to alleviate disease development or improve prognosis. Moreover, we predict that Nec-1 has the potential to protect against the complications of coronavirus disease 2019 (COVID-19). This review summarized the effect of Nec-1 in disease models and the underlying molecular mechanism, providing research evidence for its future application.

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          Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China

          Chaolin Huang, Yeming Wang, Xingwang Li … (2020)
          Summary Background A recent cluster of pneumonia cases in Wuhan, China, was caused by a novel betacoronavirus, the 2019 novel coronavirus (2019-nCoV). We report the epidemiological, clinical, laboratory, and radiological characteristics and treatment and clinical outcomes of these patients. Methods All patients with suspected 2019-nCoV were admitted to a designated hospital in Wuhan. We prospectively collected and analysed data on patients with laboratory-confirmed 2019-nCoV infection by real-time RT-PCR and next-generation sequencing. Data were obtained with standardised data collection forms shared by WHO and the International Severe Acute Respiratory and Emerging Infection Consortium from electronic medical records. Researchers also directly communicated with patients or their families to ascertain epidemiological and symptom data. Outcomes were also compared between patients who had been admitted to the intensive care unit (ICU) and those who had not. Findings By Jan 2, 2020, 41 admitted hospital patients had been identified as having laboratory-confirmed 2019-nCoV infection. Most of the infected patients were men (30 [73%] of 41); less than half had underlying diseases (13 [32%]), including diabetes (eight [20%]), hypertension (six [15%]), and cardiovascular disease (six [15%]). Median age was 49·0 years (IQR 41·0–58·0). 27 (66%) of 41 patients had been exposed to Huanan seafood market. One family cluster was found. Common symptoms at onset of illness were fever (40 [98%] of 41 patients), cough (31 [76%]), and myalgia or fatigue (18 [44%]); less common symptoms were sputum production (11 [28%] of 39), headache (three [8%] of 38), haemoptysis (two [5%] of 39), and diarrhoea (one [3%] of 38). Dyspnoea developed in 22 (55%) of 40 patients (median time from illness onset to dyspnoea 8·0 days [IQR 5·0–13·0]). 26 (63%) of 41 patients had lymphopenia. All 41 patients had pneumonia with abnormal findings on chest CT. Complications included acute respiratory distress syndrome (12 [29%]), RNAaemia (six [15%]), acute cardiac injury (five [12%]) and secondary infection (four [10%]). 13 (32%) patients were admitted to an ICU and six (15%) died. Compared with non-ICU patients, ICU patients had higher plasma levels of IL2, IL7, IL10, GSCF, IP10, MCP1, MIP1A, and TNFα. Interpretation The 2019-nCoV infection caused clusters of severe respiratory illness similar to severe acute respiratory syndrome coronavirus and was associated with ICU admission and high mortality. Major gaps in our knowledge of the origin, epidemiology, duration of human transmission, and clinical spectrum of disease need fulfilment by future studies. Funding Ministry of Science and Technology, Chinese Academy of Medical Sciences, National Natural Science Foundation of China, and Beijing Municipal Science and Technology Commission.
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            The pathogenesis and treatment of the `Cytokine Storm' in COVID-19

            Qing Ye, Bili Wang, Jianhua Mao (2020)
            Summary Cytokine storm is an excessive immune response to external stimuli. The pathogenesis of the cytokine storm is complex. The disease progresses rapidly, and the mortality is high. Certain evidence shows that, during the coronavirus disease 2019 (COVID-19) epidemic, the severe deterioration of some patients has been closely related to the cytokine storm in their bodies. This article reviews the occurrence mechanism and treatment strategies of the COVID-19 virus-induced inflammatory storm in attempt to provide valuable medication guidance for clinical treatment.
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              Reduction and Functional Exhaustion of T Cells in Patients With Coronavirus Disease 2019 (COVID-19)

              Bo Diao, Chenhui Wang, Yingjun Tan … (2020)
              Background: The outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has posed great threat to human health. T cells play a critical role in antiviral immunity but their numbers and functional state in COVID-19 patients remain largely unclear. Methods: We retrospectively reviewed the counts of T cells and serum cytokine concentration from data of 522 patients with laboratory-confirmed COVID-19 and 40 healthy controls. In addition, the expression of T cell exhaustion markers were measured in 14 COVID-19 cases. Results: The number of total T cells, CD4+ and CD8+ T cells were dramatically reduced in COVID-19 patients, especially in patients requiring Intensive Care Unit (ICU) care. Counts of total T cells, CD8+ T cells or CD4+ T cells lower than 800, 300, or 400/μL, respectively, were negatively correlated with patient survival. T cell numbers were negatively correlated to serum IL-6, IL-10, and TNF-α concentration, with patients in the disease resolution period showing reduced IL-6, IL-10, and TNF-α concentrations and restored T cell counts. T cells from COVID-19 patients had significantly higher levels of the exhausted marker PD-1. Increasing PD-1 and Tim-3 expression on T cells was seen as patients progressed from prodromal to overtly symptomatic stages. Conclusions: T cell counts are reduced significantly in COVID-19 patients, and the surviving T cells appear functionally exhausted. Non-ICU patients with total T cells counts lower than 800/μL may still require urgent intervention, even in the immediate absence of more severe symptoms due to a high risk for further deterioration in condition.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Pharmacol Res
                Journal ID (iso-abbrev): Pharmacol Res
                Title: Pharmacological Research
                Publisher: Elsevier Ltd.
                ISSN (Print): 1043-6618
                ISSN (Electronic): 1096-1186
                Publication date PMC-release: 9 November 2020
                Publication date (Print): January 2021
                Publication date (Electronic): 9 November 2020
                Volume: 163
                Page: 105297
                Affiliations
                [0005]State Key Laboratory of Oncogenes and Related Genes, Center for Single-Cell Omics, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China
                Author notes
                [* ]Corresponding author.
                Article
                Publisher Item ID: S1043-6618(20)31605-4 Publisher ID: 105297
                DOI: 10.1016/j.phrs.2020.105297
                PMC ID: 7962892
                PubMed ID: 33181319
                SO-VID: 70831de1-e3aa-4404-a1f2-aeee4fa2dff9
                Copyright © © 2020 Elsevier Ltd. All rights reserved.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                Date received : 1 September 2020
                Date revision received : 17 October 2020
                Date accepted : 3 November 2020
                Categories
                Subject: Article

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: aaa, abdominal aortic aneurysm,ad, alzheimer’s disease,aki, acute kidney injury,ali, acute lung injury,als, amyotrophic lateral sclerosis,amd, age-related macular degeneration,camkii, ca2+/calmodulin-dependent protein kinase ii,ciap1/2, cellular inhibitor of apoptosis proteins 1 and 2,covid-19, coronavirus disease 2019,cyp-d, cyclophilin-d,damps, damage-associated molecular patterns,ers, endoplasmic reticulum stress,fadd, fas associated via death domain,fhf, fulminant hepatic failure,gsh, glutathione,hd, huntington’s disease,hg, high glucose,hi, hypoxia-ischemia,hiv-1, human immunodeficiency virus type 1,hmgb1, high mobility group box 1,i/r, ischemia-reperfusion,ich, intracerebral hemorrhage,ido, indoleamine 2,3-dioxygenase,il, interleukin,ldl, low density lipoprotein,lmp, lysosomal membrane permeabilization,lps, lipopolysaccharide,mi, myocardial infarction,mlkl, mixed lineage kinase domain-like protein,mptp, mitochondrial permeability transition pore,mth-trp, methyl-thiohydantoin-tryptophan,mtor, mechanistic target of rapamycin,nec-1, necrostatin-1,nec-1i, necrostatin-1 inactive,nec-1s, necrostatin-1 stable,nf-κb, nuclear factor kappa b,ox-ldl, oxidized ldl,parp1, polymerase 1,pcd, programmed cell death,pd, parkinson’s disease,prr, pattern recognition receptor,pygl, glycogen phosphorylase,rda, rip1-dependent apoptosis,rgag, advanced glycation end products,rgcs, retinal ganglion cells,ria, rip1-indipendent apoptosis,rip1, receptor interacting protein 1,rip3, receptor interacting protein 3,ros, reactive oxygen species,rpe, retinal pigment epithelial,sah, subarachnoid hemorrhage,sci, spinal cord injury,sirs, systemic inflammatory response syndrome,tbi, traumatic brain injury,tnf, tumor necrosis factor,tnfr1, tnf receptor 1,tradd, tnfr-associated death domain,traf2, tnfr-associated factor 2,necrostatin-1,necroptosis,disease models,anti-inflammation,covid-19
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: aaa, abdominal aortic aneurysm, ad, alzheimer’s disease, aki, acute kidney injury, ali, acute lung injury, als, amyotrophic lateral sclerosis, amd, age-related macular degeneration, camkii, ca2+/calmodulin-dependent protein kinase ii, ciap1/2, cellular inhibitor of apoptosis proteins 1 and 2, covid-19, coronavirus disease 2019, cyp-d, cyclophilin-d, damps, damage-associated molecular patterns, ers, endoplasmic reticulum stress, fadd, fas associated via death domain, fhf, fulminant hepatic failure, gsh, glutathione, hd, huntington’s disease, hg, high glucose, hi, hypoxia-ischemia, hiv-1, human immunodeficiency virus type 1, hmgb1, high mobility group box 1, i/r, ischemia-reperfusion, ich, intracerebral hemorrhage, ido, indoleamine 2,3-dioxygenase, il, interleukin, ldl, low density lipoprotein, lmp, lysosomal membrane permeabilization, lps, lipopolysaccharide, mi, myocardial infarction, mlkl, mixed lineage kinase domain-like protein, mptp, mitochondrial permeability transition pore, mth-trp, methyl-thiohydantoin-tryptophan, mtor, mechanistic target of rapamycin, nec-1, necrostatin-1, nec-1i, necrostatin-1 inactive, nec-1s, necrostatin-1 stable, nf-κb, nuclear factor kappa b, ox-ldl, oxidized ldl, parp1, polymerase 1, pcd, programmed cell death, pd, parkinson’s disease, prr, pattern recognition receptor, pygl, glycogen phosphorylase, rda, rip1-dependent apoptosis, rgag, advanced glycation end products, rgcs, retinal ganglion cells, ria, rip1-indipendent apoptosis, rip1, receptor interacting protein 1, rip3, receptor interacting protein 3, ros, reactive oxygen species, rpe, retinal pigment epithelial, sah, subarachnoid hemorrhage, sci, spinal cord injury, sirs, systemic inflammatory response syndrome, tbi, traumatic brain injury, tnf, tumor necrosis factor, tnfr1, tnf receptor 1, tradd, tnfr-associated death domain, traf2, tnfr-associated factor 2, necrostatin-1, necroptosis, disease models, anti-inflammation, covid-19

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