An Epigenetic Insight into NLRP3 Inflammasome Activation in Inflammation-Related Processes

Raneros, Aroa Baragaño; Bernet, Cristian Ruiz; Flórez, Aida Bernardo; Suárez-Álvarez, Beatriz

doi:10.3390/biomedicines9111614

Cited by 22 publications

(20 citation statements)

References 139 publications

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“…Inflammasome activation is associated with rapid innate inflammatory response and leads mainly to the production of IL-1β and IL-18 [ 55 , 56 ]. The inflammation process that is triggered by the inflammasome contributes to the pathogenesis of a wide spectrum of chronic diseases, including obesity [ 51 , 57 ].…”

Section: Mechanisms Explaining the Association Between Gut Microbiota...mentioning

confidence: 99%

From Gut Microbiota through Low-Grade Inflammation to Obesity: Key Players and Potential Targets

et al. 2022

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During the last decades, the gut microbiota has gained much interest in relation to human health. Mounting evidence has shown a strict association between gut microbiota and obesity and its related diseases. Inflammation has been appointed as the driving force behind this association. Therefore, a better understanding of the mechanisms by which gut microbiota might influence inflammation in the host could pave for the identification of effective strategies to reduce inflammation-related diseases, such as obesity and obesity-related diseases. For this purpose, we carried out an extensive literature search for studies published in the English language during the last 10 years. Most relevant studies were used to provide a comprehensive view of all aspects related to the association of gut microbiota and low-grade inflammation with obesity. Accordingly, this narrative review reports the evidence on the key players supporting the role of gut microbiota in the modulation of inflammation in relation to obesity and its complications. Moreover, therapeutic approaches to reduce microbiota-related inflammation are discussed to provide potential targets for future research.

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Section: Mechanisms Explaining the Association Between Gut Microbiota...mentioning

confidence: 99%

From Gut Microbiota through Low-Grade Inflammation to Obesity: Key Players and Potential Targets

et al. 2022

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“…By contrast, extrinsic and intrinsic apoptosis activate pannexin-1 to drive NLRP3 inflammasome assembly [ 136 ], and caspase-1 initiates apoptosis in the absence of gasdermin D [ 137 ]. Finally, note that epigenetic dynamics is a key regulator of the expression of inflammasome components and its further activation [ 138 ]. Therefore, targeting mitochondrial maintenance may control cell homeostasis, and in turn, delay aging and prevent related diseases such as RA.…”

Section: Interplay Between Mitochondrial Oxidative Stress Metabolic S...mentioning

confidence: 99%

“…In fact, the key drivers of RA synovitis, TNF and IL-1, reprogram the epigenomic landscape of FLS by altering chromatin and contributing then to induce unremitting expression of arthritogenic genes in RA synoviocytes [ 233 , 234 , 235 ]. Additionally, note as different epigenetic changes are involved into NLRP3 inflammasome activation [ 138 ]. Histone modification and micro-RNA are too involved in epigenetic regulation in the pathogenesis of RA.…”

Section: Interplay Between Mitochondrial and Epigenetic Mechanisms In Ramentioning

confidence: 99%

Mitochondrial Dysfunction and Oxidative Stress in Rheumatoid Arthritis

2022

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Control of excessive mitochondrial oxidative stress could provide new targets for both preventive and therapeutic interventions in the treatment of chronic inflammation or any pathology that develops under an inflammatory scenario, such as rheumatoid arthritis (RA). Increasing evidence has demonstrated the role of mitochondrial alterations in autoimmune diseases mainly due to the interplay between metabolism and innate immunity, but also in the modulation of inflammatory response of resident cells, such as synoviocytes. Thus, mitochondrial dysfunction derived from several danger signals could activate tricarboxylic acid (TCA) disruption, thereby favoring a vicious cycle of oxidative/mitochondrial stress. Mitochondrial dysfunction can act through modulating innate immunity via redox-sensitive inflammatory pathways or direct activation of the inflammasome. Besides, mitochondria also have a central role in regulating cell death, which is deeply altered in RA. Additionally, multiple evidence suggests that pathological processes in RA can be shaped by epigenetic mechanisms and that in turn, mitochondria are involved in epigenetic regulation. Finally, we will discuss about the involvement of some dietary components in the onset and progression of RA.

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“…The inflammasome is a key player in activating caspase-1 and stimulating the inflammatory cytokines interleukin IL-1β and IL-18 [ 44 ]. The trigger of inflammasomes starts when immune cells face pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs) by pattern recognition receptors (PRRs) [ 45 ]. During recent years, it was demonstrated that NLRC4, caspase-1, ASC and IL-18 are elevated in the aged brain, confirming its key role in the innate immune response [ 46 , 47 ].…”

Section: Cytokines and Neuroinflammationmentioning

confidence: 99%

Neuro-Inflammaging and Psychopathological Distress

et al. 2022

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Inflammaging is a low degree of chronic and systemic tissue inflammation associated with aging, and is intimately linked to pro-inflammatory mediators. These substances are involved in the pathogenesis of chronic inflammatory diseases and related psychopathological symptoms. When inflammation and aging affect the brain, we use the term neuro-inflammaging. In this review, we focused on the neuro-inflammatory process typical of advanced ages and the related psychopathological symptoms, with particular attention to understanding the immune-pathogenetic mechanisms involved and the potential use of immunomodulatory drugs in the control of clinical psychological signs. Inflammation and CNS were demonstrated being intimately linked in the neuro-inflammatory loop. IL-1, IL-6, TNF-a, COX and PGE are only partially responsible. BBB permeability and the consequent oxidative stress resulting from tissue damage make the rest. Some authors elaborated the “theory of cytokine-induced depression”. Inflammation has a crucial role in the onset symptoms of psychopathological diseases as it is capable of altering the metabolism of biogenic monoamines involved in their pathogenesis. In recent years, NSAIDs as an adjunct therapy in the treatment of relevant psychopathological disorders associated with chronic inflammatory conditions demonstrated their efficacy. Additionally, novel molecules have been studied, such as adalimumab, infliximab, and etanercept showing antidepressant and anxiolytic promising results. However, we are only at the beginning of a new era characterized by the use of biological drugs for the treatment of inflammatory and autoimmune diseases, and this paper aims to stimulate future studies in such a direction.

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An Epigenetic Insight into NLRP3 Inflammasome Activation in Inflammation-Related Processes

Cited by 22 publications

References 139 publications

From Gut Microbiota through Low-Grade Inflammation to Obesity: Key Players and Potential Targets

From Gut Microbiota through Low-Grade Inflammation to Obesity: Key Players and Potential Targets

Mitochondrial Dysfunction and Oxidative Stress in Rheumatoid Arthritis

Neuro-Inflammaging and Psychopathological Distress

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