Lycopene Ameliorates Atrazine-Induced Pyroptosis in Spleen via Suppressing the Ox-mtDNA/Nlrp3 Inflammasome Pathway

2021 ◽  
Author(s):  
Shi-Yong Zhu ◽  
Jian-Ying Guo ◽  
Jin-Yang Li ◽  
Xueyan Dai ◽  
Xue-Nan Li ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Metabolic Disorders ◽  
Cellular Stress ◽  
Integration Point ◽  
Extracellular Stimuli

Nlrp3 is a vital integration point of diverse extracellular stimuli and cellular stress. However, inappropriate activation of Nlrp3 results in progression of autoinflammatory and metabolic disorders. Atrazine, using widely in...

scholarly journals Stk24 protects against obesity-associated metabolic disorders by disrupting the NLRP3 inflammasome

Cell Reports ◽  
2021 ◽  
Vol 35 (8) ◽  
pp. 109161
Author(s):  
Qiang Qin ◽  
Jia’nan Shou ◽  
Mengjie Li ◽  
Meidi Gu ◽  
Zhuoxian Meng ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Metabolic Disorders

scholarly journals The NLRP3 Inflammasome as a Novel Player of the Intercellular Crosstalk in Metabolic Disorders

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Elisa Benetti ◽  
Fausto Chiazza ◽  
Nimesh S. A. Patel ◽  
Massimo Collino
Keyword(s):  
Chronic Inflammation ◽  
Nlrp3 Inflammasome ◽  
Metabolic Disorders ◽  
Inflammasome Activation ◽  
Nucleotide Binding Domain ◽  
Metabolic Inflammation ◽  
Nlrp3 Inflammasome Activation ◽  
Leucine Rich Repeat Protein

The combination of obesity and type 2 diabetes is a serious health problem, which is projected to afflict 300 million people worldwide by 2020. Both clinical and translational laboratory studies have demonstrated that chronic inflammation is associated with obesity and obesity-related conditions such as insulin resistance. However, the precise etiopathogenetic mechanisms linking obesity to diabetes remain to be elucidated, and the pathways that mediate this phenomenon are not fully characterized. One of the most recently identified signaling pathways, whose activation seems to affect many metabolic disorders, is the “inflammasome,” a multiprotein complex composed of NLRP3 (nucleotide-binding domain and leucine-rich repeat protein 3), ASC (apoptosis-associated speck-like protein containing a CARD), and procaspase-1. NLRP3 inflammasome activation leads to the processing and secretion of the proinflammatory cytokines interleukin- (IL-) 1βand IL-18. The goal of this paper is to review new insights on the effects of the NLRP3 inflammasome activation in the complex mechanisms of crosstalk between different organs, for a better understanding of the role of chronic inflammation in metabolic disease pathogenesis. We will provide here a perspective on the current research on NLRP3 inflammasome, which may represent an innovative therapeutic target to reverse the detrimental metabolic consequences of the metabolic inflammation.

scholarly journals Salvianolic Acid A Ameliorates Early-Stage Atherosclerosis Development by Inhibiting NLRP3 Inflammasome Activation in Zucker Diabetic Fatty Rats

Molecules ◽  
2020 ◽  
Vol 25 (5) ◽  
pp. 1089 ◽  
Author(s):  
Quanxin Ma ◽  
Qinqin Yang ◽  
Jiaojiao Chen ◽  
Chen Yu ◽  
Lizong Zhang ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Metabolic Disorders ◽  
Salvia Miltiorrhiza ◽  
Blood Cholesterol ◽  
Inflammasome Activation ◽  
Salvianolic Acid ◽  
Salvianolic Acid A ◽  
Zucker Diabetic Fatty Rats ◽  
Zdf Rats ◽  
Anti Inflammatory

Salvianolic acid A (SAA), an important bioactive polyphenolic acid found in Salvia miltiorrhiza Bunge, may be used for treating metabolic disorders due to its anti-inflammatory activity. Since chronic inflammation plays an important role in type 2 diabetes mellitus (T2DM) complicated with atherosclerosis (AS), SAA may have beneficial effects on AS. Here, we evaluated the effects of SAA on metabolic disorders in male Zucker diabetic fatty (ZDF) rats induced by a high-fat diet and Vitamin D3 injections. Compared with the model group, the SAA high dosage (1 mg/kg) group exhibited decreased hemoglobin A1C levels but unchanged blood glucose levels. The disrupted lipid profiles were ameliorated by SAA, with significantly decreased levels of blood cholesterol, LDL-C and triglyceride. The protective effects of SAA against early AS were further confirmed by histopathological examination of aortic tissues. In addition, we observed that SAA decreased serum hs-CRP levels and suppressed the activation of NLRP3 inflammasome and NF-κB signaling in aortic tissues of ZDF rats. Collectively, our results demonstrate the potential of SAA to alleviate AS and T2DM in ZDF rats as a result of its anti-inflammatory effects.

scholarly journals NLRP3 Inflammasome Activation in Adipose Tissues and Its Implications on Metabolic Diseases

2020 ◽  
Vol 21 (11) ◽  
pp. 4184 ◽  
Author(s):  
Kelvin Ka-Lok Wu ◽  
Samson Wing-Ming Cheung ◽  
Kenneth King-Yip Cheng
Keyword(s):  
Adipose Tissue ◽  
Nlrp3 Inflammasome ◽  
Metabolic Disorders ◽  
Immune Cell ◽  
Diabetic Patients ◽  
Inflammasome Activation ◽  
Low Grade ◽  
Adipose Tissues ◽  
Adipose Tissue Dysfunction ◽  
Nlrp3 Inflammasome Activation

Adipose tissue is an active endocrine and immune organ that controls systemic immunometabolism via multiple pathways. Diverse immune cell populations reside in adipose tissue, and their composition and immune responses vary with nutritional and environmental conditions. Adipose tissue dysfunction, characterized by sterile low-grade chronic inflammation and excessive immune cell infiltration, is a hallmark of obesity, as well as an important link to cardiometabolic diseases. Amongst the pro-inflammatory factors secreted by the dysfunctional adipose tissue, interleukin (IL)-1β, induced by the NLR family pyrin domain-containing 3 (NLRP3) inflammasome, not only impairs peripheral insulin sensitivity, but it also interferes with the endocrine and immune functions of adipose tissue in a paracrine manner. Human studies indicated that NLRP3 activity in adipose tissues positively correlates with obesity and its metabolic complications, and treatment with the IL-1β antibody improves glycaemia control in type 2 diabetic patients. In mouse models, genetic or pharmacological inhibition of NLRP3 activation pathways or IL-1β prevents adipose tissue dysfunction, including inflammation, fibrosis, defective lipid handling and adipogenesis, which in turn alleviates obesity and its related metabolic disorders. In this review, we summarize both the negative and positive regulators of NLRP3 inflammasome activation, and its pathophysiological consequences on immunometabolism. We also discuss the potential therapeutic approaches to targeting adipose tissue inflammasome for the treatment of obesity and its related metabolic disorders.

Endoplasmic reticulum stress and NLRP3 inflammasome: Crosstalk in cardiovascular and metabolic disorders

2019 ◽  
Vol 234 (9) ◽  
pp. 14773-14782 ◽  
Author(s):  
Ting Ji ◽  
Yuehu Han ◽  
Wenwen Yang ◽  
Baoping Xu ◽  
Meng Sun ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Nlrp3 Inflammasome ◽  
Metabolic Disorders

scholarly journals Reciprocal Crosstalk Between Autophagic and Endocrine Signaling in Metabolic Homeostasis

2016 ◽  
Vol 38 (1) ◽  
pp. 69-102 ◽  
Author(s):  
Rohit A. Sinha ◽  
Brijesh K. Singh ◽  
Paul M. Yen
Keyword(s):  
Metabolic Disorders ◽  
Basic Mechanism ◽  
Endocrine Regulation ◽  
Metabolic Homeostasis ◽  
Extracellular Stimuli ◽  
Initial Discovery ◽  
And Function ◽  
Endocrine Signaling ◽  
Present Understanding ◽  
Insight Into

Abstract Autophagy is a cellular quality control and energy-providing process that is under strict control by intra- and extracellular stimuli. Recently, there has been an exponential increase in autophagy research and its implications for mammalian physiology. Autophagy deregulation is now being implicated in many human diseases, and its modulation has shown promising results in several preclinical studies. However, despite the initial discovery of autophagy as a hormone-regulated process by De Duve in the early 1960s, endocrine regulation of autophagy still remains poorly understood. In this review, we provide a critical summary of our present understanding of the basic mechanism of autophagy, its regulation by endocrine hormones, and its contribution to endocrine and metabolic homeostasis under physiological and pathological settings. Understanding the cross-regulation of hormones and autophagy on endocrine cell signaling and function will provide new insight into mammalian physiology as well as promote the development of new therapeutic strategies involving modulation of autophagy in endocrine and metabolic disorders.

scholarly journals The Role of the Interplay Between Autophagy and NLRP3 Inflammasome in Metabolic Disorders

2021 ◽  
Vol 9 ◽  
Author(s):  
Shuangyu Lv ◽  
Honggang Wang ◽  
Xiaotian Li
Keyword(s):  
Nlrp3 Inflammasome ◽  
Metabolic Disorders ◽  
Interleukin 1 ◽  
Basic Research ◽  
Interleukin 1 Beta ◽  
Cell Composition ◽  
Pyrin Domain ◽  
Receptor Family ◽  
Oligomerization Domain

Autophagy is an important and conserved cellular pathway in which cells transmit cytoplasmic contents to lysosomes for degradation. It plays an important role in maintaining the balance of cell composition synthesis, decomposition and reuse, and participates in a variety of physiological and pathological processes. The nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome can induce the maturation and secretion of Interleukin-1 beta (IL-1β) and IL-18 by activating caspase-1. It is involved in many diseases. In recent years, the interplay between autophagy and NLRP3 inflammasome has been reported to contribute to many diseases including metabolic disorders related diseases. In this review, we summarized the recent studies on the interplay between autophagy and NLRP3 inflammasome in metabolic disorders to provide ideas for the relevant basic research in the future.

The NLRP3 inflammasome: Role in metabolic disorders and regulation by metabolic pathways

2018 ◽  
Vol 419 ◽  
pp. 8-19 ◽  
Author(s):  
Danlu Jiang ◽  
Sheng Chen ◽  
Ruyu Sun ◽  
Xue Zhang ◽  
Di Wang
Keyword(s):  
Nlrp3 Inflammasome ◽  
Metabolic Pathways ◽  
Metabolic Disorders

scholarly journals Role of NLRP3 Inflammasome Activation in Obesity-Mediated Metabolic Disorders

2021 ◽  
Vol 18 (2) ◽  
pp. 511
Author(s):  
Kaiser Wani ◽  
Hind AlHarthi ◽  
Amani Alghamdi ◽  
Shaun Sabico ◽  
Nasser M. Al-Daghri
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Nlrp3 Inflammasome ◽  
Metabolic Disorders ◽  
Metabolic Diseases ◽  
Protein Complexes ◽  
Inflammasome Activation ◽  
Low Grade ◽  
Nlrp3 Inflammasome Activation ◽  
Specific Inhibitors

NLRP3 inflammasome is one of the multimeric protein complexes of the nucleotide-binding domain, leucine-rich repeat (NLR)-containing pyrin and HIN domain family (PYHIN). When activated, NLRP3 inflammasome triggers the release of pro-inflammatory interleukins (IL)-1β and IL-18, an essential step in innate immune response; however, defective checkpoints in inflammasome activation may lead to autoimmune, autoinflammatory, and metabolic disorders. Among the consequences of NLRP3 inflammasome activation is systemic chronic low-grade inflammation, a cardinal feature of obesity and insulin resistance. Understanding the mechanisms involved in the regulation of NLRP3 inflammasome in adipose tissue may help in the development of specific inhibitors for the treatment and prevention of obesity-mediated metabolic diseases. In this narrative review, the current understanding of NLRP3 inflammasome activation and regulation is highlighted, including its putative roles in adipose tissue dysfunction and insulin resistance. Specific inhibitors of NLRP3 inflammasome activation which can potentially be used to treat metabolic disorders are also discussed.

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