Special Issue "Inflammasomes as the Target of Pharmacotherapy"
Deadline for manuscript submissions: 20 December 2023 | Viewed by 4725
Interests: neurodegenerative diseases; Alzheimer’s disease; dementia; cell biology; molecular biology; ageing; therapeutics and rehabilitation
As a sensor of infections and external stimuli, inflammasomes play a key role in the pathological process of various diseases . Inflammasomes are intracellular multimeric complex molecules  including: i) canonical inflammasomes (NLRP3, NLRC4, and AIM2) that serve as a platform to engage pro-caspase-1, which becomes active caspase-1 and processes pro-interleukin-1β (IL-1β) and pro-IL-18 to generate their active forms, inducing pyroptosis, a pro-inflammatory form of cell death [2,3–5]; and ii) noncanonical inflammasomes that activate caspase-11 (mouse) or caspase-4/5 (human) without cleaving pro-IL-1β [1,6].
Available compounds act mainly by inhibiting the products of inflammasome activation, for example, by impeding the biological effects of downstream interleukins [7,8], but given the lack of effective drugs in the therapy of different inflammatory chronic conditions, it is becoming particularly pressing to understand and provide a potentially practical pharmacological approach for treating NLRP3-driven diseases.
In this Special Issue, we aim to gather research from experts in the field that highlights therapeutic agents and strategies to identify future discoveries and therapies for “inflammasomes”-mediated inflammatory disorders.
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 Rathinam, V. A., Vanaja, S. K. & Fitzgerald, K. A. Regulation of inflammasome signaling. Nat. Immunol. 13, 333–342 (2012).
 Thornberry, N. A. et al. A novel heterodimeric cysteine protease is required for interleukin-1 beta processing in monocytes. Nature 356, 768–774 (1992).
 Hagar, J. A., Powell, D. A., Aachoui, Y., Ernst, R. K. & Miao, E. A. Cytoplasmic LPS activates caspase-11: implications in TLR4-independent endotoxic shock. Science 341, 1250–1253 (2013).
 La Rosa F, Saresella M, Marventano I, Piancone F, Ripamonti E, Al-Daghri N, Bazzini C, Zoia CP, Conti E, Ferrarese C, et al. Stavudine Reduces NLRP3 Inflammasome Activation and Modulates Amyloid-β Autophagy. J. Alzheimers Dis. 72, 401-412 (2019).
 La Rosa F, Mancuso R, Agostini S, Piancone F, Marventano I, Saresella M, Hernis A, Fenoglio C, Galimberti D, Scarpini E, Clerici M. Pharmacological and Epigenetic Regulators of NLRP3 Inflammasome Activation in Alzheimer's Disease. Pharmaceuticals 14, 1187 (2021).
Dr. Francesca La Rosa
Dr. Marina Saresella
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