Chronic Heart Failure and Inflammation

Circulation Research, Journal Year: 2016, Volume and Issue: 119(1), P. 159 - 176

Published: June 24, 2016

As a greater proportion of patients survive their initial cardiac insult, medical systems worldwide are being faced with an ever-growing need to understand the mechanisms behind pathogenesis chronic heart failure (HF). There is wealth information about role inflammatory cells and pathways during acute injury reparative processes that subsequently activated. We discuss different causes lead HF development how sum responses only sets trajectory for disease progression. Unfortunately, comparatively little known contribution immune system once has been set, established-which clinically represents majority patients. It associated circulating cytokines can predict clinical outcomes, yet causative inflammation plays in progression not well defined, trials target aspects have largely negative. This review will present what currently both humans animal models as means highlight gap our knowledge base requires further examination.

Language: Английский

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Common neurodegenerative pathways in obesity, diabetes, and Alzheimer's disease

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Journal Year: 2016, Volume and Issue: 1863(5), P. 1037 - 1045

Published: May 6, 2016

Language: Английский

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Pharmacological Inhibitors of the NLRP3 Inflammasome

Frontiers in Immunology, Journal Year: 2019, Volume and Issue: 10

Published: Oct. 25, 2019

Inflammasomes play a crucial role in innate immunity by serving as signaling platforms which deal with plethora of pathogenic products and cellular associated stress damage. By far, the best studied most characterized inflammasome is NLRP3 inflammasome, consists (nucleotide-binding domain leucine-rich repeat (NLR) pyrin containing receptor 3), ASC (apoptosis-associated speck-like protein caspase recruitment domain), procaspase-1. Activation mediated highly diverse stimuli. Upon activation, recruits adapter protein, procaspase-1 resulting its cleavage inducing maturation, secretion inflammatory cytokines pyroptosis. However, aberrant activation implicated various diseases including diabetes, atherosclerosis, metabolic syndrome, cardiovascular, neurodegenerative diseases; raising tremendous clinical interest exploring potential inhibitors inflammasome. Recent investigations have disclosed pathway were validated through

Language: Английский

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AMPK as a Therapeutic Target for Treating Metabolic Diseases

Trends in Endocrinology and Metabolism, Journal Year: 2017, Volume and Issue: 28(8), P. 545 - 560

Published: June 21, 2017

Language: Английский

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Inflammasome activation and function in liver disease

Nature Reviews Gastroenterology & Hepatology, Journal Year: 2015, Volume and Issue: 12(7), P. 387 - 400

Published: June 9, 2015

Language: Английский

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Molecular and Cellular Mechanisms of Cardiovascular Disorders in Diabetes

Circulation Research, Journal Year: 2016, Volume and Issue: 118(11), P. 1808 - 1829

Published: May 26, 2016

The clinical correlations linking diabetes mellitus with accelerated atherosclerosis, cardiomyopathy, and increased post-myocardial infarction fatality rates are increasingly understood in mechanistic terms. multiple mechanisms discussed this review seem to share a common element: prolonged increases reactive oxygen species (ROS) production diabetic cardiovascular cells. Intracellular hyperglycemia causes excessive ROS production. This activates nuclear poly(ADP-ribose) polymerase, which inhibits GAPDH, shunting early glycolytic intermediates into pathogenic signaling pathways. polymerase also reduce sirtuin, PGC-1α, AMP-activated protein kinase activity. These changes cause decreased mitochondrial biogenesis, production, disturbed circadian clock synchronization of glucose lipid metabolism. Excessive facilitates transport proatherogenic transcription factors, the neutrophil enzyme initiating NETosis, peptidylarginine deiminase 4, NOD-like receptor family, pyrin domain-containing 3 inflammasome. Insulin resistance cardiomyocyte by increasing fatty acid flux oxidation. stimulates overexpression PPARα translocation forkhead box O 1, cardiomyopathy. shift balance between fusion fission favor fission, reducing metabolic capacity efficiency electron chain ATP synthesis. Mitochondrial oxidative stress plays central role angiotensin II–induced gap junction remodeling arrhythmogenesis. contribute sudden death diabetics after myocardial post-translational modifications, ryanodine phosphorylation downregulation sarco-endoplasmic reticulum Ca ++ -ATPase transcription. Increased depress autonomic ganglion synaptic transmission oxidizing nAch α3 subunit, potentially contributing risk fatal cardiac arrhythmias associated neuropathy.

Language: Английский

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Interleukin-18 in Health and Disease

International Journal of Molecular Sciences, Journal Year: 2019, Volume and Issue: 20(3), P. 649 - 649

Published: Feb. 2, 2019

Interleukin (IL)-18 was originally discovered as a factor that enhanced IFN-γ production from anti-CD3-stimulated Th1 cells, especially in the presence of IL-12. Upon stimulation with Ag plus IL-12, naïve T cells develop into IL-18 receptor (IL-18R) expressing which increase response to stimulation. Therefore, IL-12 is commitment induces development cells. In contrast, proinflammatory cytokine facilitates type 1 responses. However, without but IL-2, stimulates NK CD4+ NKT and established produce IL-3, IL-9, IL-13. Furthermore, together mast basophils IL-4, IL-13, chemical mediators such histamine. various cell types has pleiotropic functions. member IL-1 family cytokines. demonstrates unique function by binding specific expressed on this review article, we will focus features health disease experimental animals humans.

Language: Английский

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The Warburg effect then and now: From cancer to inflammatory diseases

BioEssays, Journal Year: 2013, Volume and Issue: 35(11), P. 965 - 973

Published: Sept. 20, 2013

Inflammatory immune cells, when activated, display much the same metabolic profile as a glycolytic tumor cell. This involves shift in metabolism away from oxidative phosphorylation towards aerobic glycolysis, phenomenon known Warburg effect. The result of this change macrophages is to rapidly provide ATP and intermediates for biosynthesis inflammatory proteins. In addition, rise certain tricarboxylic acid cycle occurs notably citrate lipid biosynthesis, succinate, which activates transcription factor Hypoxia‐inducible factor. review we take look at emerging evidence role effect responses. reprogramming pathways macrophages, dendritic T cells could have relevance pathogenesis diseases might novel therapeutic strategies.

Language: Английский

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Gut Microbiota as a Trigger for Metabolic Inflammation in Obesity and Type 2 Diabetes

Frontiers in Immunology, Journal Year: 2020, Volume and Issue: 11

Published: Oct. 16, 2020

The gut microbiota has been linked to the development of obesity and type 2 diabetes (T2D). underlying mechanisms as how intestinal may contribute T2D are only partly understood. It becomes progressively clear that is characterized by a chronic state low-grade inflammation, which insulin resistance. Here, we review current evidence microbiota, metabolites they produce, could drive resistance in T2D, possibly initiating an inflammatory response. First, will summarize major findings about immunological microbial changes these metabolic diseases. Next, give detailed view on have implicated inflammation. Lastly, critically discuss clinical studies focus interaction between immune system disease. Overall, there strong tripartite host metabolism critical partaker pathophysiology T2D.

Language: Английский

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Inflammation: the link between comorbidities, genetics, and Alzheimer’s disease

Journal of Neuroinflammation, Journal Year: 2018, Volume and Issue: 15(1)

Published: Sept. 24, 2018

Alzheimer’s disease (AD) is a neurodegenerative disorder, most cases of which lack clear causative event. This has made the difficult to characterize and, thus, diagnose. Although some are genetically linked, there many diseases and lifestyle factors that can lead an increased risk developing AD, including traumatic brain injury, diabetes, hypertension, obesity, other metabolic syndromes, in addition aging. Identifying common trends between these conditions could enhance our understanding AD development more effective treatments. immune system one body’s key defense mechanisms, chronic inflammation been increasingly linked with several age-related diseases. Moreover, it now well accepted important role onset progression AD. In this review, different inflammatory signals associated its will be outlined demonstrate how may influencing individual susceptibility Our goal bring attention potential shared presented by during successful

Language: Английский

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