scholarly journals Pyroptosis: A New Frontier in Kidney Diseases

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Ke-jia Zhang ◽  
Qi Wu ◽  
Shi-min Jiang ◽  
Lei Ding ◽  
Chao-xia Liu ◽  
...  
Keyword(s):  
Kidney Diseases ◽  
Inflammatory Factors ◽  
Pathogenic Role ◽  
New Frontier ◽  
Membrane Perforation ◽  
Noncanonical Pathway ◽  
And Function ◽  
Cell Collapse ◽  
Novel Therapeutic

Pyroptosis is a pattern of programmed cell death that significantly differs from apoptosis and autophagy in terms of cell morphology and function. The process of pyroptosis is characterized predominantly by the formation of gasdermin protein family-mediated membrane perforation, cell collapse, and the release of inflammatory factors, including IL-1β and IL-18. In recent years, with the rise of pyroptosis research, scholars have devoted time to study the mechanism of pyroptosis in kidney-related diseases. Pyroptosis is probably involved in kidney diseases through two pathways: the caspase-1-mediated canonical pathway and the caspase-4/5/11-mediated noncanonical pathway. In addition, some scholars have identified targets for the treatment of kidney-related diseases from the viewpoint of pyroptosis and developed corresponding medicines, which may become a recommendation for prognosis, targeted treatment, and clinical diagnosis of kidney diseases. This paper focuses on the up-to-date advances in the field of pyroptosis, especially on the key pathogenic role of pyroptosis in the development and progression of kidney diseases. It presents a more in-depth understanding of the pathogenesis of kidney diseases and introduces novel therapeutic targets for the prevention and clinical treatment of kidney diseases.

Von Willebrand disease and Weibel-Palade bodies

2010 ◽  
Vol 30 (03) ◽  
pp. 150-155 ◽  
Author(s):  
J. W. Wang ◽  
J. Eikenboom
Keyword(s):  
Platelet Adhesion ◽  
Coagulation Factor ◽  
Von Willebrand Disease ◽  
Inflammatory Factors ◽  
Limited Data ◽  
Storage Organelle ◽  
And Function ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryVon Willebrand factor (VWF) is a pivotal haemostatic protein mediating platelet adhesion to injured endothelium and carrying coagulation factor VIII (FVIII) in the circulation to protect it from premature clearance. Apart from the roles in haemostasis, VWF drives the formation of the endothelial cell specific Weibel-Palade bodies (WPBs), which serve as a regulated storage of VWF and other thrombotic and inflammatory factors. Defects in VWF could lead to the bleeding disorder von Willebrand disease (VWD).Extensive studies have shown that several mutations identified in VWD patients cause an intracellular retention of VWF. However, the effects of such mutations on the formation and function of its storage organelle are largely unknown. This review gives an overview on the role of VWF in WPB biogenesis and summarizes the limited data on the WPBs formed by VWD-causing mutant VWF.

The Role of the CX3CL1-CX3CR1 Axis in Renal Disease

2021 ◽  
Author(s):  
Diana Hamdan ◽  
Lisa A. Robinson
Keyword(s):  
Therapeutic Potential ◽  
Kidney Diseases ◽  
Transmembrane Protein ◽  
Soluble Form ◽  
Protective Effects ◽  
Chronic Kidney Diseases ◽  
The Family ◽  
Soluble Species ◽  
And Function

Excessive infiltration of immune cells into the kidney is a key feature of acute and chronic kidney diseases. The family of chemokines are key drivers of this process. CX3CL1 (fractalkine) is one of two unique chemokines synthesized as a transmembrane protein which undergoes proteolytic cleavage to generate a soluble species. Through interacting with its cognate receptor, CX3CR1, CX3CL1 was originally shown to act as a conventional chemoattractant in the soluble form, and as an adhesion molecule in the transmembrane form. Since then, other functions of CX3CL1 beyond leukocyte recruitment have been described, including cell survival, immunosurveillance, and cell-mediated cytotoxicity. This review summarizes diverse roles of CX3CL1 in kidney disease and potential uses as a therapeutic target and novel biomarker. As the CX3CL1-CX3CR1 axis has been shown to contribute to both detrimental and protective effects in various kidney diseases, a thorough understanding of how the expression and function of CX3CL1 are regulated is needed to unlock its therapeutic potential.

The role of BA AS signaling molecules and novel therapeutic targets to protect endothelial metabolism and function against obesity

2020 ◽  
Vol 315 ◽  
pp. e57
Author(s):  
A. Jomard ◽  
O. Chavez-Talavera ◽  
A. Tailleux ◽  
F. Ruschitzka ◽  
A. Von Eckardstein ◽  
...  
Keyword(s):  
Therapeutic Targets ◽  
Signaling Molecules ◽  
And Function ◽  
Novel Therapeutic

scholarly journals The CXCL1-CXCR2 Axis Mediates Tubular Injury in Diabetic Nephropathy Through the Regulation of the Inflammatory Response

2021 ◽  
Vol 12 ◽  
Author(s):  
Hanfen Tang ◽  
Ming Yang ◽  
Yinghong Liu ◽  
Hong Liu ◽  
Lin Sun ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Inflammatory Response ◽  
Renal Damage ◽  
Essential Role ◽  
Inflammatory Factors ◽  
Tubular Injury ◽  
Inflammatory Damage ◽  
First Time ◽  
Novel Therapeutic

Diabetic nephropathy (DN) is one of the most severe complications of diabetes. Inflammation mediated by inflammatory factors is thought to accelerate the progression of renal damage in DN. However, which inflammatory factors mediate the inflammatory response in DN remains unclear. In this study, we determined that the CXCL1-mediated inflammatory response may play an essential role in DN progression through bioassays. Subsequently, we observed that the expression of CXCL1 and its receptor (CXCR2) was significantly increased in the kidneys of mice with HFD + STZ induced diabetes and DN patients. In addition, inhibition of the CXCL1/CXCR2 axis by repertaxin alleviates renal inflammation and pathological damage in the kidneys of db/db mice. Finally, we noted that the CXCL1/CXCR2 axis might lead to inflammatory damage through phosphorylated NF-κB and further activate the NLRP3 inflammasome. Our results revealed the role of the CXCL1/CXCR2 axis in DN progression for the first time, which may be a novel therapeutic target for DN.

scholarly journals The role of endothelial glycocalyx in health and disease

2019 ◽  
Vol 12 (5) ◽  
pp. 611-619 ◽  
Author(s):  
Onur Yilmaz ◽  
Baris Afsar ◽  
Alberto Ortiz ◽  
Mehmet Kanbay
Keyword(s):  
State Of The Art ◽  
Kidney Diseases ◽  
Structure And Function ◽  
The Body ◽  
Endothelial Glycocalyx ◽  
Surrogate Markers ◽  
Disease States ◽  
Health And Disease ◽  
And Function

AbstractThe endothelium is the largest organ in the body and recent studies have shown that the endothelial glycocalyx (eGCX) plays a major role in health and disease states. The integrity of eGCX is vital for homoeostasis and disruption of its structure and function plays a major role in several pathologic conditions. An increased understanding of the numerous pathophysiological roles of eGCX may lead to the development of potential surrogate markers for endothelial injury or novel therapeutic targets. This review provides a state-of-the-art update on the structure and function of the eGCX, emphasizing the current understanding of interorgan crosstalk between the eGCX and other organs that might also contribute to the pathogenesis of kidney diseases.

scholarly journals Podocyte Lipotoxicity in CKD

Kidney360 ◽  
2021 ◽  
Vol 2 (4) ◽  
pp. 755-762
Author(s):  
Jin-Ju Kim ◽  
Sydney S. Wilbon ◽  
Alessia Fornoni
Keyword(s):  
Lipid Metabolism ◽  
Lipid Accumulation ◽  
Kidney Diseases ◽  
Treatment Options ◽  
The United States ◽  
Differentiated Cells ◽  
Filtration Barrier ◽  
And Function ◽  
Cellular Components ◽  
Novel Therapeutic

CKD represents the ninth most common cause of death in the United States but, despite this large health burden, treatment options for affected patients remain limited. To remedy this, several relevant pathways have been identified that may lead to novel therapeutic options. Among them, altered renal lipid metabolism, first described in 1982, has been recognized as a common pathway in clinical and experimental CKD of both metabolic and nonmetabolic origin. This observation has led many researchers to investigate the cause of this renal parenchyma lipid accumulation and its downstream effect on renal structure and function. Among key cellular components of the kidney parenchyma, podocytes are terminally differentiated cells that cannot be easily replaced when lost. Clinical and experimental evidence supports a role of reduced podocyte number in the progression of CKD. Given the importance of the podocytes in the maintenance of the glomerular filtration barrier and the accumulation of TG and cholesterol-rich lipid droplets in the podocyte and glomerulus in kidney diseases that cause CKD, understanding the upstream cause and downstream consequences of lipid accumulation in podocytes may lead to novel therapeutic opportunities. In this review, we hope to consolidate our understanding of the causes and consequences of dysregulated renal lipid metabolism in CKD development and progression, with a major focus on podocytes.

scholarly journals The Role of Regulatory B cells in Kidney Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Wang Long ◽  
Hedong Zhang ◽  
Wenjia Yuan ◽  
Gongbin Lan ◽  
Zhi Lin ◽  
...  
Keyword(s):  
B Cells ◽  
Autoimmune Diseases ◽  
Kidney Diseases ◽  
Specific Marker ◽  
Protective Effects ◽  
Regulatory B Cells ◽  
Multiple Phenotypes ◽  
Therapeutic Value ◽  
And Function

B cells, commonly regarded as proinflammatory antibody-producing cells, are detrimental to individuals with autoimmune diseases. However, in recent years, several studies have shown that regulatory B (Breg) cells, an immunosuppressive subset of B cells, may exert protective effects against autoimmune diseases by secretion of inhibitory cytokines such as IL-10. In practice, Breg cells are identified by their production of immune-regulatory cytokines, such as IL-10, TGF-β, and IL-35, however, no specific marker or Breg cell-specific transcription factor has been identified. Multiple phenotypes of Breg cells have been found, whose functions vary according to their phenotype. This review summarizes the discovery, phenotypes, development, and function of Breg cells and highlights their potential therapeutic value in kidney diseases.

Tu1950 Pathogenic Role of IL-33-Mediated Eosinophil Infiltration and Function in Experimental IBD

2012 ◽  
Vol 142 (5) ◽  
pp. S-885
Author(s):  
Carlo De Salvo ◽  
Xiao-Ming Wang ◽  
Benedetta Mattioli ◽  
Luca Pastorelli ◽  
Rekha R. Garg ◽  
...  
Keyword(s):  
Eosinophil Infiltration ◽  
Pathogenic Role ◽  
And Function

scholarly journals Osteoblast role in the pathogenesis of rheumatoid arthritis

2021 ◽  
Vol 48 (3) ◽  
pp. 2843-2852
Author(s):  
S. Berardi ◽  
A. Corrado ◽  
N. Maruotti ◽  
D. Cici ◽  
F. P. Cantatore
Keyword(s):  
Rheumatoid Arthritis ◽  
Bone Loss ◽  
Current Knowledge ◽  
Interleukin 1 ◽  
Inflammatory Factors ◽  
Bone Homeostasis ◽  
Factor Α ◽  
And Function ◽  
Maximal Reduction

AbstractIn the pathogenesis of several rheumatic diseases, such as rheumatoid arthritis, spondyloarthritis, osteoarthritis, osteoporosis, alterations in osteoblast growth, differentiation and activity play a role. In particular, in rheumatoid arthritis bone homeostasis is perturbed: in addition to stimulating the pathologic bone resorption process performed by osteoclasts in course of rheumatoid arthritis, proinflammatory cytokines (such as Tumor Necrosis factor-α, Interleukin-1) can also inhibit osteoblast differentiation and function, resulting in net bone loss. Mouse models of rheumatoid arthritis showed that complete resolution of inflammation (with maximal reduction in the expression of pro-inflammatory factors) is crucial for bone healing, performed by osteoblasts activity. In fact, abnormal activity of factors and systems involved in osteoblast function in these patients has been described. A better understanding of the pathogenic mechanisms involved in osteoblast dysregulation could contribute to explain the generalized and focal articular bone loss found in rheumatoid arthritis. Nevertheless, these aspects have not been frequently and directly evaluated in studies. This review article is focused on analysis of the current knowledge about the role of osteoblast dysregulation occurring in rheumatoid arthritis: a better knowledge of these mechanisms could contribute to the realization of new therapeutic strategies.

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