scholarly journals Glucocorticoid-Induced Leucine Zipper (GILZ) in Cardiovascular Health and Disease

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2155
Author(s):  
Donato Cappetta ◽  
Oxana Bereshchenko ◽  
Eleonora Cianflone ◽  
Francesco Rossi ◽  
Carlo Riccardi ◽  
...  
Keyword(s):  
Leucine Zipper ◽  
Cardiovascular Health ◽  
Immune Cell ◽  
Inflammatory Diseases ◽  
Cellular Adhesion ◽  
Cellular Adhesion Molecules ◽  
Autoimmune And Inflammatory Diseases ◽  
Inflammatory Processes ◽  
Cardiovascular Biology

Glucocorticoids (GCs) are essential in regulating functions and homeostasis in many biological systems and are extensively used to treat a variety of conditions associated with immune/inflammatory processes. GCs are among the most powerful drugs for the treatment of autoimmune and inflammatory diseases, but their long-term usage is limited by severe adverse effects. For this reason, to envision new therapies devoid of typical GC side effects, research has focused on expanding the knowledge of cellular and molecular effects of GCs. GC-induced leucine zipper (GILZ) is a GC-target protein shown to mediate several actions of GCs, including inhibition of the NF-κB and MAPK pathways. GILZ expression is not restricted to immune cells, and it has been shown to play a regulatory role in many organs and tissues, including the cardiovascular system. Research on the role of GILZ on endothelial cells has demonstrated its ability to modulate the inflammatory cascade, resulting in a downregulation of cytokines, chemokines, and cellular adhesion molecules. GILZ also has the capacity to protect myocardial cells, as its deletion makes the heart, after a deleterious stimulus, more susceptible to apoptosis, immune cell infiltration, hypertrophy, and impaired function. Despite these advances, we have only just begun to appreciate the relevance of GILZ in cardiovascular homeostasis and dysfunction. This review summarizes the current understanding of the role of GILZ in modulating biological processes relevant to cardiovascular biology.

scholarly journals Regulatory T cells in acute and chronic kidney diseases

2018 ◽  
Vol 314 (5) ◽  
pp. F679-F698 ◽  
Author(s):  
Rahul Sharma ◽  
Gilbert R. Kinsey
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cell Activation ◽  
Cell Function ◽  
Immune Cell ◽  
Inflammatory Diseases ◽  
Kidney Diseases ◽  
Peripheral Tolerance ◽  
Autoimmune And Inflammatory Diseases

Foxp3-expressing CD4+ regulatory T cells (Tregs) make up one subset of the helper T cells (Th) and are one of the major mechanisms of peripheral tolerance. Tregs prevent abnormal activation of the immune system throughout the lifespan, thus protecting from autoimmune and inflammatory diseases. Recent studies have elucidated the role of Tregs beyond autoimmunity. Tregs play important functions in controlling not only innate and adaptive immune cell activation, but also regulate nonimmune cell function during insults and injury. Inflammation contributes to a multitude of acute and chronic diseases affecting the kidneys. This review examines the role of Tregs in pathogenesis of renal inflammatory diseases and explores the approaches for enhancing Tregs for prevention and therapy of renal inflammation.

scholarly journals Therapeutic Targeting of Immune Cell Autophagy in Multiple Sclerosis: Russian Roulette or Silver Bullet?

2021 ◽  
Vol 12 ◽  
Author(s):  
Guan Yang ◽  
Luc Van Kaer
Keyword(s):  
Multiple Sclerosis ◽  
Immune Cell ◽  
Inflammatory Diseases ◽  
Chronic Inflammatory Disease ◽  
Nerve Fibers ◽  
Therapeutic Approaches ◽  
Autoimmune Encephalomyelitis ◽  
Autoimmune And Inflammatory Diseases ◽  
The Central Nervous System

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) in which the immune system damages the protective insulation surrounding nerve fibers that project from neurons. The pathological hallmark of MS is multiple areas of myelin loss accompanied by inflammation within the CNS, resulting in loss of cognitive function that ultimately leads to paralysis. Recent studies in MS have focused on autophagy, a cellular self-eating process, as a potential target for MS treatment. Here, we review the contribution of immune cell autophagy to the pathogenesis of experimental autoimmune encephalomyelitis (EAE), the prototypic animal model of MS. A better understanding of the role of autophagy in different immune cells to EAE might inform the development of novel therapeutic approaches in MS and other autoimmune and inflammatory diseases.

THE ROLE OF CELLULAR ADHESION MOLECULES IN SURGERY

1995 ◽  
Vol 65 (12) ◽  
pp. 838-847 ◽  
Author(s):  
A. F. Breidahl ◽  
M. J. Hickey ◽  
A. G. Stewart ◽  
P. G. Hayward ◽  
W. A. Morrison
Keyword(s):  
Adhesion Molecules ◽  
Cellular Adhesion ◽  
Cellular Adhesion Molecules

scholarly journals Succinate Is an Inflammation-Induced Immunoregulatory Metabolite in Macrophages

Metabolites ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 372 ◽  
Author(s):  
Karl J. Harber ◽  
Kyra E. de Goede ◽  
Sanne G. S. Verberk ◽  
Elisa Meinster ◽  
Helga E. de Vries ◽  
...  
Keyword(s):  
Immune Responses ◽  
Immune Cells ◽  
Immune Cell ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Cell Phenotype ◽  
Independent Manner ◽  
Inflammatory Macrophages ◽  
Necrosis Factor

Immunometabolism revealed the crucial role of cellular metabolism in controlling immune cell phenotype and functions. Macrophages, key immune cells that support progression of numerous inflammatory diseases, have been well described as undergoing vast metabolic rewiring upon activation. The immunometabolite succinate particularly gained a lot of attention and emerged as a crucial regulator of macrophage responses and inflammation. Succinate was originally described as a metabolite that supports inflammation via distinct routes. Recently, studies have indicated that succinate and its receptor SUCNR1 can suppress immune responses as well. These apparent contradictory effects might be due to specific experimental settings and particularly the use of distinct succinate forms. We therefore compared the phenotypic and functional effects of distinct succinate forms and receptor mouse models that were previously used for studying succinate immunomodulation. Here, we show that succinate can suppress secretion of inflammatory mediators IL-6, tumor necrosis factor (TNF) and nitric oxide (NO), as well as inhibit Il1b mRNA expression of inflammatory macrophages in a SUCNR1-independent manner. We also observed that macrophage SUCNR1 deficiency led to an enhanced inflammatory response without addition of exogenous succinate. While our study does not reveal new mechanistic insights into how succinate elicits different inflammatory responses, it does indicate that the inflammatory effects of succinate and its receptor SUCNR1 in macrophages are clearly context dependent.

Biomarkers in vesicoureteral reflux: an overview

2020 ◽  
Vol 14 (8) ◽  
pp. 683-696
Author(s):  
Flávia C Valério ◽  
Renata D Lemos ◽  
Ana L de C Reis ◽  
Letícia P Pimenta ◽  
Érica LM Vieira ◽  
...  
Keyword(s):  
Vesicoureteral Reflux ◽  
Renal Scarring ◽  
Reflux Nephropathy ◽  
Serum Levels ◽  
Cellular Adhesion ◽  
High Grade ◽  
Epigenetic Factors ◽  
Cellular Adhesion Molecules ◽  
Potential Biomarkers

Aim: This article aimed to review the role of cytokines, chemokines, growth factors and cellular adhesion molecules as biomarkers for vesicoureteral reflux (VUR) and reflux nephropathy (RN). Methods: We reviewed articles from 1979 onward by searching PubMed and Scopus utilizing the combination of words: ‘VUR’ or ‘RN’ and each one of the biomarkers. Results: Genetic, inflammatory, fibrogenic, environmental and epigenetic factors responsible for renal scarring need to be better understood. TGF-β, IL-10, IL-6, IL-8 and TNF seem to exert a role in VUR particularly in RN based on the current literature. Serum levels of procalcitonin have been also associated with high-grade VUR and RN. These molecules should be more intensively evaluated as potential biomarkers for renal scarring in VUR. Conclusion: Further studies are necessary to define which molecules will really be of utility in clinical decisions and as therapeutic targets for VUR and RN.

scholarly journals The Role of Poly(ADP-ribose) Polymerase-1 in Rheumatoid Arthritis

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Samuel García ◽  
Carmen Conde
Keyword(s):  
Rheumatoid Arthritis ◽  
Septic Shock ◽  
Dna Repair ◽  
Beneficial Effect ◽  
Current Knowledge ◽  
Inflammatory Diseases ◽  
Genomic Stability ◽  
Inflammatory Processes ◽  
Parp 1

Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear enzyme with a crucial role in the maintenance of genomic stability. In addition to the role of PARP-1 in DNA repair, multiple studies have also demonstrated its involvement in several inflammatory diseases, such as septic shock, asthma, atherosclerosis, and stroke, as well as in cancer. In these diseases, the pharmacological inhibition of PARP-1 has shown a beneficial effect, suggesting that PARP-1 regulates their inflammatory processes. In recent years, we have studied the role of PARP-1 in rheumatoid arthritis, as have other researchers, and the results have shown that PARP-1 has an important function in the development of this disease. This review summarizes current knowledge on the effects of PARP-1 in rheumatoid arthritis.

scholarly journals DIAGNOSTIC ROLE OF BONE SCINTIGRAPHY IN EARLY PROGNOSIS OF PARAENDOPROSTHETIC COMPLICATIONS IN ARTHROPLASTY OF HIP AND KNIEE JOINTS

2018 ◽  
pp. 73-78
Author(s):  
P. Korol ◽  
M. Tkachenko
Keyword(s):  
Bone Scintigraphy ◽  
Inflammatory Diseases ◽  
Knee Joints ◽  
Three Phase ◽  
Static Phase ◽  
Diagnostic Role ◽  
Specific Accumulation ◽  
Inflammatory Processes ◽  
Kinetics Of

For 10 years, we studied the diagnostic role of three-phase bone scintigraphy (3-f BS) in the early prognosis of paraendoprosthetic complications in patients with degenerative-dystrophic and infectious-inflammatory diseases of the hip and knee joints. Using 3-f BS, the kinetic radionuclide parameters of inclusion and distribution of radiopharmaceutical (RP) in the projection of affected joints were evaluated. It was determined that the kinetics of osteotropic RP in the foci of fixation of affected joints in infectious and inflammatory processes is characterized by the predominance of retention and specific accumulation of the drug in the early and delayed static phase of 3-f BS in comparison with foci of fixing RP in degenerative-dystrophic lesions, which correlates with the differences destructively-reparative processes in them.According to the results of the analysis of the kinetic parameters, a radionuclide model of the dynamics of inclusion and distribution of RP in septic and aseptic joint lesions has been developed.

scholarly journals Genetics and Inflammation in Endometriosis: Improving Knowledge for Development of New Pharmacological Strategies

2021 ◽  
Vol 22 (16) ◽  
pp. 9033
Author(s):  
Elisa Giacomini ◽  
Sabrina Minetto ◽  
Letizia Li Li Piani ◽  
Luca Pagliardini ◽  
Edgardo Somigliana ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Immune Cells ◽  
Immune Cell ◽  
Extracellular Vesicle ◽  
Cellular Adhesion ◽  
Therapeutic Approaches ◽  
Therapeutic Alternative ◽  
Per Se ◽  
Functional Pathways

According to a rich body of literature, immune cell dysfunctions, both locally and systemically, and an inflammatory environment characterize all forms of endometriosis. Alterations in transcripts and proteins involved in the recruitment of immune cells, in the interaction between cytokines and their receptors, cellular adhesion and apoptosis have been demonstrated in endometriotic lesions. The objective of this narrative review is to provide an overview of the components and mechanisms at the intersection between inflammation and genetics that may constitute vanguard therapeutic approaches in endometriosis. The GWAS technology and pathway-based analysis highlighted the role of the MAPK and the WNT/β-catenin cascades in the pathogenesis of endometriosis. These signaling pathways have been suggested to interfere with the disease establishment via several mechanisms, including apoptosis, migration and angiogenesis. Extracellular vesicle-associated molecules may be not only interesting to explain some aspects of endometriosis progression, but they may also serve as therapeutic regimens per se. Immune/inflammatory dysfunctions have always represented attractive therapeutic targets in endometriosis. These would be even more interesting if genetic evidence supported the involvement of functional pathways at the basis of these alterations. Targeting these dysfunctions through next-generation inhibitors can constitute a therapeutic alternative for endometriosis.

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