The role of NLRP3 inflammasome in aging and age-related diseases

Abstract

The gradual aging of the global population has led to a surge in age-related diseases, which seriously threaten human health. Researchers are dedicated to understanding and coping with the complexities of aging, constantly uncovering the substances and mechanism related to aging like chronic low-grade inflammation. The NOD-like receptor protein 3 (NLRP3), a key regulator of the innate immune response, recognizes molecular patterns associated with pathogens and injury, initiating an intrinsic inflammatory immune response. Dysfunctional NLRP3 is linked to the onset of related diseases, particularly in the context of aging. Therefore, a profound comprehension of the regulatory mechanisms of the NLRP3 inflammasome in aging-related diseases holds the potential to enhance treatment strategies for these conditions. In this article, we review the significance of the NLRP3 inflammasome in the initiation and progression of diverse aging-related diseases. Furthermore, we explore preventive and therapeutic strategies for aging and related diseases by manipulating the NLRP3 inflammasome, along with its upstream and downstream mechanisms.

Inflammaging, immunosenescence, and cardiovascular aging: insights into long COVID implications

“…NLRP3 activation triggers the production of pro-inflammatory cytokines IL-1β and IL-18. This chronic inflammation contributes to diseases such as atherosclerosis, type 2 diabetes, and Alzheimer's disease ( 24 , 25 ). Among the various downstream pro-inflammatory pathways activated by the NLRP3 inflammasome, IL-1β and IL-18 emerge as potential contributors to inflammaging.…”

The Effects of Caloric Restriction on Inflammatory Targets in the Prostates of Aged Rats

“…The intricate process of inflammation is strictly linked to the activation of NLRP3 inflammasomes (multiprotein complexes belonging to innate immunity), which, triggered by pathogen-and danger-associated molecular patterns via TLR4, leads to the production of IL-1β, thereby initiating a potent inflammatory response [8]. Robust evidence describes NLRP inflammasome dysfunction during aging and suggests that the activation and hyperactivation of NLRP3 inflammasomes strongly contribute to inflammaging and the onset and progression of age-related diseases [9]. To strengthen this evidence, in vivo studies showed that NLRP3 pathway inhibition mitigates age-related organ damage [10][11][12].…”