Adjuvant strategies for prevention of glomerulosclerosis

McCarty, Mark F.

doi:10.1016/j.mehy.2004.11.048

Cited by 30 publications

(27 citation statements)

References 297 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Diabetes and hypertension are currently the two principal causes of CKD (2), among other causes such as infectious glomerulonephritis, renal vasculitis, ureteral obstruction, genetic alterations, autoimmune diseases (1) and drugs (3,4). In general, diabetes causes glomerular hypertension by reducing the afferent arteriolar resistance while stimulating the efferent arterioles (2).…”

Section: Renal Fibrosis: Aetiology and Pathophysiologymentioning

confidence: 99%

“…In general, diabetes causes glomerular hypertension by reducing the afferent arteriolar resistance while stimulating the efferent arterioles (2). Thus, elevated glomerular capillary pressure is one of the major factors in progressive renal sclerosis (5).…”

Section: Renal Fibrosis: Aetiology and Pathophysiologymentioning

confidence: 99%

“…The end-stage of renal disease is manifested by the presence of glomerulosclerosis, vascular sclerosis and tubulointerstitial fibrosis. Indeed, glomerulosclerosis is initially attributable to the disproportionate production of ground substance proteins by mesangial cells, associated with a reduction in the extracellular proteolytic activity generated by these cells (2). In this sense, the excessive glomerular production of transforming growth factor (TGF)-β, the key cytokine in the development of glomerulosclerosis and tubulointerstitial fibrosis (11), stimulates mesangial cells (2,12), and is probably the most potent inducer of epithelialmesenchymal transition (13).…”

Section: Renal Fibrosis: Aetiology and Pathophysiologymentioning

confidence: 99%

“…Indeed, glomerulosclerosis is initially attributable to the disproportionate production of ground substance proteins by mesangial cells, associated with a reduction in the extracellular proteolytic activity generated by these cells (2). In this sense, the excessive glomerular production of transforming growth factor (TGF)-β, the key cytokine in the development of glomerulosclerosis and tubulointerstitial fibrosis (11), stimulates mesangial cells (2,12), and is probably the most potent inducer of epithelialmesenchymal transition (13). Activation of TGFβ results in a self-maintaining cycle of matrix deposition, through an increase in protein synthesis and a decrease in matrix protein degradation, resulting in persistent tissue injury (11,14).…”

Section: Renal Fibrosis: Aetiology and Pathophysiologymentioning

confidence: 99%

“…The diminution of this cytokine bioactivity reduces ECM deposition and the development of fibrosis in experimental renal injury (11). On the other hand, an increase in oxidative stress has been associated with increased mesangial expression of TGFβ (2) and also stimulation by angiotensin II (Ang II) (15). Endothelial and mesangial oxidant stress related to diabetes and systemic hypertension may also interfere with the production of glomerular nitric oxide, possibly reducing the activity of nitric oxide and thus impairing its protective effect in the process of glomerulosclerosis (2).…”

Section: Renal Fibrosis: Aetiology and Pathophysiologymentioning

confidence: 99%

See 4 more Smart Citations

Pathophysiological Mechanisms of Renal Fibrosis: A Review of Animal Models and Therapeutic Strategies

2017

View full text Add to dashboard Cite

Abstract. Chronic kidney disease (CKD) is a long-term condition in which theChronic kidney disease (CKD) represents a serious hazard to human health, and has a high prevalence. In developed countries, it is estimated that more than 10% of adults present some degree of CKD (1). Despite a varied initial evolution, which is related to the diversity of its aetiologies -namely genetics, autoimmune-related infections, environmental factors, diet, and drugs -progressive renal disease frequently results in renal fibrosis and finally in renal failure. The mechanisms implicated in renal fibrosis are still poorly understood, and existing therapies are ineffective or only slightly successful, hence it is essential to understand the pathophysiological mechanisms underlying the usual development of CKD, and to discover and better understand new strategies for treating this disease. In order to study the biopathology of this disease and to evaluate new treatments, animal models are required. The perfect animal model for renal disease research should have human-like renal anatomy, haemodynamics and physiology, as well as enabling the determination of relevant renal, biochemical and haemodynamic parameters. In all probability, no species can consistently meet all these requirements, and the experimental plan and other constraints often determine the choice of animal models for particular research applications. With this in mind, this review aims to describe and analyze animal models of renal fibrosis and suggest new areas of research. Renal Fibrosis: Aetiology and PathophysiologyDiabetes and hypertension are currently the two principal causes of CKD (2), among other causes such as infectious glomerulonephritis, renal vasculitis, ureteral obstruction, genetic alterations, autoimmune diseases (1) and drugs (3, 4). In general, diabetes causes glomerular hypertension by reducing the afferent arteriolar resistance while stimulating the efferent arterioles (2). Thus, elevated glomerular capillary pressure is one of the major factors in progressive renal sclerosis (5). Diabetes and hypertension gradually lead to glomerular expansion, which causes endothelial dysfunction and haemodynamic changes: loss of the glomerular basement membrane electric charge and its thickening, a decreased number of podocytes, foot-process effacement and mesangial distension have been shown to 1

show abstract

Section: Renal Fibrosis: Aetiology and Pathophysiologymentioning

confidence: 99%

Section: Renal Fibrosis: Aetiology and Pathophysiologymentioning

confidence: 99%

Section: Renal Fibrosis: Aetiology and Pathophysiologymentioning

confidence: 99%

Section: Renal Fibrosis: Aetiology and Pathophysiologymentioning

confidence: 99%

Section: Renal Fibrosis: Aetiology and Pathophysiologymentioning

confidence: 99%

See 3 more Smart Citations

Pathophysiological Mechanisms of Renal Fibrosis: A Review of Animal Models and Therapeutic Strategies

2017

View full text Add to dashboard Cite

show abstract

Targeting Oxidant Stress as a Strategy for Preventing Vascular Complications of Diabetes and Metabolic Syndrome

McCarty¹,

Inoguchi

2008

Nutraceuticals, Glycemic Health and Type 2 Diabetes

View full text Add to dashboard Cite

A study on correlation between oxidative stress parameters and inflammatory markers in type 2 diabetic patients with kidney dysfunction in north Indian population

Neelofar

Arif

Arafat

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

Background Research reports support the statement that oxidative stress and inflammation are well‐known risk factors for chronic kidney disease (CKD) in patients with diabetes. This study was designed to ascertain the associated role of oxidative stress parameters and inflammatory markers in diabetes and related CKD among the north Indian population. Methods The study was divided into three groups as healthy subjects (group 1), patients with diabetes without complication (group 2), and with CKD (group 3). Serum levels of malondialdehyde (MDA) and nitric oxide (NO), superoxide dismutase (SOD), catalase (CAT), and glutathione reductase (GR) content were estimated in all individuals. Inflammatory cytokines interleukin‐6 (IL‐6) and tumor necrosis factor‐α (TNF‐α)‐α were determined by enzyme‐linked immuno‐sorbent assay. Results MDA, protein carbonyl, and NO were significantly elevated in patients with type 2 diabetes as compared with healthy subjects (P ≤ 0.05). Total thiols content were found to be significantly decreased in patients with diabetes with CKD. The activity of antioxidant enzymes SOD, CAT, and GR showed a significant suppression in patients with type 2 diabetes with or without CKD as compared with healthy subjects. Nevertheless, the levels of proinflammatory cytokines IL‐6 and TNF‐α were significantly upregulated ( P ≤ 0.05) as compared with healthy subjects. Conclusion Determination of antioxidant defense parameters and inflammatory markers contributes to understand the relationship between oxidative stress and inflammation on the development and prevention of chronic kidney disease in Indian patients with diabetes.

show abstract

Adjuvant strategies for prevention of glomerulosclerosis

Cited by 30 publications

References 297 publications

Pathophysiological Mechanisms of Renal Fibrosis: A Review of Animal Models and Therapeutic Strategies

Pathophysiological Mechanisms of Renal Fibrosis: A Review of Animal Models and Therapeutic Strategies

Targeting Oxidant Stress as a Strategy for Preventing Vascular Complications of Diabetes and Metabolic Syndrome

A study on correlation between oxidative stress parameters and inflammatory markers in type 2 diabetic patients with kidney dysfunction in north Indian population

Contact Info

Product

Resources

About