The Role of NLRP3 Inflammasome in Lupus Nephritis

Oliveira, Camila Barbosa Lyra de; Lima, Camilla Albertina Dantas de; Vajgel, Gisele; Sandrin-Garcia, Paula

doi:10.3390/ijms222212476

Cited by 35 publications

(27 citation statements)

References 89 publications

(114 reference statements)

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“…After NLRP3 is activated, downstream molecules are recruited and assembled to form the NLRP3 inflammasome. Studies have shown that the NLRP3 inflammasome is overactivated in lupus nephritis, which promotes the exacerbation of inflammation and the progression of LN [ 29 , 31 ]. Based on previous findings, our results suggested that CD36 promotes podocyte injury by activating the NLRP3 inflammasome in lupus nephritis.…”

Section: Discussionmentioning

confidence: 99%

CD36 aggravates podocyte injury by activating NLRP3 inflammasome and inhibiting autophagy in lupus nephritis

et al. 2022

Cell Death Dis

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A major cause of proteinuria in lupus nephritis (LN) is podocyte injury, and determining potential therapeutic targets to prevent podocyte injury is important from a clinical perspective in the treatment of LN. CD36 is involved in podocyte injury in several glomerulopathies and was reported to be a vital candidate gene in LN. Here, we determined the role of CD36 in the podocyte injury of LN and the underlying mechanisms. We observed that CD36 and NLRP3 (NLR family pyrin domain containing 3) were upregulated in the podocytes of lupus nephritis patients and MRL/lpr mice with renal impairment. In vitro, CD36, NLRP3 inflammasome, and autophagy were elevated accompanied with increased podocyte injury stimulated by IgG extracted from lupus nephritis patients compared that from healthy donors. Knocking out CD36 with the CRISPR/cas9 system decreased the NLRP3 inflammasome levels, increased the autophagy levels and alleviated podocyte injury. By enhancing autophagy, NLRP3 inflammasome was decreased and podocyte injury was alleviated. These results demonstrated that, in lupus nephritis, CD36 promoted podocyte injury by activating NLRP3 inflammasome and inhibiting autophagy by enhancing which could decrease NLRP3 inflammasome and alleviate podocyte injury.

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Section: Discussionmentioning

confidence: 99%

CD36 aggravates podocyte injury by activating NLRP3 inflammasome and inhibiting autophagy in lupus nephritis

et al. 2022

Cell Death Dis

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“…The cause of autoimmunity is multifactorial, but interplay between various immune cells is critical [ 2 ]. Aberrant IFN signaling, activation of the NLRP3 inflammasome, as well as B cells and Th17 cells, and even hyperactivation of cytototoxic CD8 + T cells is noted [ 162 , 163 , 164 , 165 ]. Also, T and natural killer cells from SLE patients show higher intracellular ROS levels of than B cells from healthy controls; at the same time, Keap1 and Nrf2 levels are elevated as an antioxidant defense mechanism [ 166 ].…”

Section: Role Of Nrf2 Agonism In Chronic Inflammatory Diseasesmentioning

confidence: 99%

Recent Advances in Understanding Nrf2 Agonism and Its Potential Clinical Application to Metabolic and Inflammatory Diseases

Kim

Jeon

2022

IJMS

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Oxidative stress is a major component of cell damage and cell fat, and as such, it occupies a central position in the pathogenesis of metabolic disease. Nuclear factor-erythroid-derived 2-related factor 2 (Nrf2), a key transcription factor that coordinates expression of genes encoding antioxidant and detoxifying enzymes, is regulated primarily by Kelch-like ECH-associated protein 1 (Keap1). However, involvement of the Keap1–Nrf2 pathway in tissue and organism homeostasis goes far beyond protection from cellular stress. In this review, we focus on evidence for Nrf2 pathway dysfunction during development of several metabolic/inflammatory disorders, including diabetes and diabetic complications, obesity, inflammatory bowel disease, and autoimmune diseases. We also review the beneficial role of current molecular Nrf2 agonists and summarize their use in ongoing clinical trials. We conclude that Nrf2 is a promising target for regulation of numerous diseases associated with oxidative stress and inflammation. However, more studies are needed to explore the role of Nrf2 in the pathogenesis of metabolic/inflammatory diseases and to review safety implications before therapeutic use in clinical practice.

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“…The second signal is induced by PAMPs and DAMPs, which convert pro-caspase-1 to caspase by inducing the oligomerization of NLRP3. The resulting activated caspase-1 induces cell lysis or pyroptosis [39]. In particular, NLRP3 is involved in the pathogenesis or progression of kidney disease.…”

Section: Nod-like Receptors (Nlrs) As Pattern-recognition Receptors (...mentioning

confidence: 99%

“…In particular, NLRP3 is involved in the pathogenesis or progression of kidney disease. Ischemic reperfusion kidney injury induces cell damage or death by secreting DAMPs, which are also involved in rhabdomyolysis-associated acute kidney injury, as well as in lupus nephritis and systemic lupus erythematosus [39]. In addition, hypomethylation of NOD-1 and NOD-2, resulting in their aberrant expression, has been associated with chronic inflammatory diseases such as inflammatory bowel disease and rheumatoid arthritis.…”

Section: Nod-like Receptors (Nlrs) As Pattern-recognition Receptors (...mentioning

confidence: 99%

The Roles of NOD-like Receptors in Innate Immunity in Otitis Media

You

Kim

Lee

et al. 2022

IJMS

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Acute otitis media (AOM) can persist or lead to various complications in individuals in which the innate immune system is impaired. In this context, impaired expression of nucleotide-binding oligomerization domain (NOD)-like receptor (NLR), an intracellular pathogen-recognition receptor (PRR), is involved in the etiology of OM in humans and animals, affecting its development, severity, chronicity, recurrence, and associated complications. To assess this relationship, we reviewed literature reports relating NLR expression patterns with the pathophysiology and clinical features of OM in the larger context of impaired innate immunity. We summarized the results of published studies on the expression of NLRs in animals and humans in acute otitis media (AOM), otitis media with effusion (OME), chronic otitis media (COM) with cholesteatoma, and COM without cholesteatoma. NLRs were expressed mainly in association with bacterial infection in AOM, OME, COM with cholesteatoma, and COM without cholesteatoma. In addition, expression of NLRs was affected by the presence or absence of bacteria, fluid characteristics, disease recurrence, tissue type, and repeated surgery. Various factors of the innate immune system are involved in the pathogenesis of OM in the middle ear. NLRs are expressed in AOM, OME, COM with cholesteatoma, and COM without cholesteatoma. Impaired NLR expression induced the development, chronicity and recurrence of OM and exacerbated associated complications, indicating that NLRs have important roles in the pathogenesis of OM.

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The Role of NLRP3 Inflammasome in Lupus Nephritis

Cited by 35 publications

References 89 publications

CD36 aggravates podocyte injury by activating NLRP3 inflammasome and inhibiting autophagy in lupus nephritis

CD36 aggravates podocyte injury by activating NLRP3 inflammasome and inhibiting autophagy in lupus nephritis

Recent Advances in Understanding Nrf2 Agonism and Its Potential Clinical Application to Metabolic and Inflammatory Diseases

The Roles of NOD-like Receptors in Innate Immunity in Otitis Media

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