Unwinding the modalities of necrosome activation and necroptosis machinery in neurological diseases

Gupta, Rohan; Smita, Kumari; Tripathi, Rahul; Ambasta, Rashmi K.; Kumar, Pravir

doi:10.1016/j.arr.2023.101855

Cited by 12 publications

(8 citation statements)

References 312 publications

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“…TAK1 has been showed to activate NF-κB, JNK/MAPK and p38/MAPK signaling pathways [8], at the same time, all of which play a role in neuronal death [49,50]. Previous studies have showed that aberrant NF-κB, JNK/MAPK and p38/MAPK signaling could induce neuronal death and involve in the pathogenesis of many central nervous system diseases, such as Alzheimer's disease [51][52][53] and stroke [54,55]. In this study, we detected these proteins and found that their expressions changed when TAK1 was knocked down or overexpressed.…”

Section: Discussionmentioning

confidence: 99%

TAK1 Improves Cognitive Function via Suppressing RIPK1-Driven Neuronal Apoptosis and Necroptosis in Rats with Chronic Hypertension

Yang

Sun

et al. 2023

Aging and disease

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Chronic hypertension is a major risk factor for cognitive impairment, which can promote neuroinflammation and neuronal loss in the central nervous system. Transforming growth factor β-activated kinase 1 (TAK1) is a key molecular component in determining cell fate and can be activated by inflammatory cytokines. This study aimed to investigate the role of TAK1 in mediating neuronal survival in the cerebral cortex and hippocampus under chronic hypertensive conditions. To that end, we used stroke-prone renovascular hypertension rats (RHRSP) as chronic hypertension models. Adeno-associated virus (AAV) designed to overexpress or knock down TAK1 expression were injected into the lateral ventricles of rats and the subsequent effects on cognitive function and neuronal survival under chronic hypertensive conditions were assessed. We found that, TAK1 knockdown in RHRSP markedly increased neuronal apoptosis and necroptosis and induced cognitive impairment, which could be reversed by Nec-1s, an inhibitor of receptor interacting protein kinase 1 (RIPK1). In contrast, overexpression of TAK1 in RHRSP significantly suppressed neuronal apoptosis and necroptosis and improved cognitive function. Further knockdown of TAK1 in sham-operated rats received similar phenotype with RHRSP. The results have been verified in vitro. In this study, we provide in vivo and in vitro evidence that TAK1 improves cognitive function by suppressing RIPK1-driven neuronal apoptosis and necroptosis in rats with chronic hypertension.

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Section: Discussionmentioning

confidence: 99%

TAK1 Improves Cognitive Function via Suppressing RIPK1-Driven Neuronal Apoptosis and Necroptosis in Rats with Chronic Hypertension

Yang

Sun

et al. 2023

Aging and disease

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“…Enhancement in Parkinson's Disease Management: The application of AI technology in the management of Parkinson's Disease (PD) demonstrates its potential in understanding protein degradation mechanisms [ 91 , 92 ]. AI technologies, such as machine learning and data mining, have been used to identify and describe protein degradation pathways involved in PD, providing potential targets for developing new therapeutic interventions.…”

Section: Future Outlook and Challengesmentioning

confidence: 99%

Biobanks in chronic disease management: A comprehensive review of strategies, challenges, and future directions

Xu,

Liang,

Chen

et al. 2024

Heliyon

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“…H + and Clion shows positive and negative effects, respectively, on the reaction rate, whereas the kinetics of the reaction was left unaffected by the variation of the ionic strength of the medium. 101 Gowda and his colleagues investigated the kinetics behind the oxidation of piperazine, 1-methylpiperazine, and 1ethylpiperazine by bromamine-T (BAT) in buffered acidic medium at 303 K (Scheme 73). 102 The reaction follows first-order kinetics in terms of [BAT]0 and [piperazine]0, and inverse fractional-order kinetics with respect to [H + ].…”

Section: Scheme 72 Oxidation Of Amido Black By Bat or Catmentioning

confidence: 99%

Bromamine-T (TsNBrNa): A Biologically Significant, Versatile Bromo-Organic Reagent

Kashyap¹,

Phukan²

2023

Synlett

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Bromamine-T (BAT) is a distinguished member of a special class of compounds called organic haloamines, possessing oxidising properties. It can act as the source of halonium ions, hypohalite species, and N-anions, along with the display of basic as well as nucleophilic properties. Bromamine-T finds wide application as an efficient reagent for various organic transformations such as aminobromination, amination, oxidation etc., under mild conditions with minimum toxicity. Moreover, due to its immense biological significance, this reagent is piquing the interest of numerous researchers.

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Unwinding the modalities of necrosome activation and necroptosis machinery in neurological diseases

Cited by 12 publications

References 312 publications

TAK1 Improves Cognitive Function via Suppressing RIPK1-Driven Neuronal Apoptosis and Necroptosis in Rats with Chronic Hypertension

TAK1 Improves Cognitive Function via Suppressing RIPK1-Driven Neuronal Apoptosis and Necroptosis in Rats with Chronic Hypertension

Biobanks in chronic disease management: A comprehensive review of strategies, challenges, and future directions

Bromamine-T (TsNBrNa): A Biologically Significant, Versatile Bromo-Organic Reagent

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