Acute renal failure. III. The role of growth factors in the process of renal regeneration and repair

2000 ◽  
Vol 279 (1) ◽  
pp. F3-F11 ◽  

This review, which is the final installment in a series devoted to controversial issues in acute renal failure (ARF) (3, 47), will examine available information regarding the role of growth factors in ARF. In general, studies in this area have fallen into two broad categories: 1) those that have examined the renal expression of genes encoding growth factors or transcriptional factors associated with the growth response that is induced after ARF, and 2) those that have examined the efficacy of exogenously administered growth factors in accelerating recovery of renal function in experimental models of ARF. Despite the vast amount of information that has accumulated in these two areas of investigation, our understanding of the mechanisms involved in the process of regeneration and repair after ARF, and the role of growth factors in this response, remains rudimentary. This overview, contributed to by a number of experts in the field, is designed to summarize present knowledge and to highlight potentially fertile areas for future research in this area.

2020 ◽  
Author(s):  
Iwona Bronisz-Budzyńska ◽  
Magdalena Kozakowska ◽  
Paulina Podkalicka ◽  
Neli Kachamakova-Trojanowska ◽  
Agnieszka Łoboda ◽  
...  

Abstract The nuclear factor erythroid 2-related factor 2 (Nrf2) is considered as a master cytoprotective factor regulating the expression of genes encoding anti-oxidant, anti-inflammatory, and detoxifying proteins. The role of Nrf2 in the pathophysiology of skeletal muscles has been evaluated in different experimental models, however, due to inconsistent data, we aimed to investigate how Nrf2 transcriptional deficiency (Nrf2tKO) affects muscle functions both in an acute and chronic injury. The acute muscle damage was induced in mice of two genotypes – WT and Nrf2tKO mice by cardiotoxin (CTX) injection. To investigate the role of Nrf2 in chronic muscle pathology, mdx mice that share genetic, biochemical, and histopathological features with Duchenne muscular dystrophy (DMD) were crossed with mice lacking transcriptionally active Nrf2 and double knockouts (mdx/Nrf2tKO) were generated. To worsen the dystrophic phenotype, the analysis of disease pathology was also performed in aggravated conditions, by applying a long-term treadmill test. We have observed slightly increased muscle degeneration in Nrf2tKO mice after CTX treatment. Nevertheless, transcriptional ablation of Nrf2 in mdx mice did not significantly aggravate the most deleterious, pathological hallmarks of DMD related to degeneration, inflammation, fibrotic scar formation, angiogenesis, and the number and proliferation of satellite cells in non-exercised conditions. On the other hand, upon chronic exercises, the degeneration and inflammatory infiltration of the gastrocnemius muscle, but not diaphragm, turned to be increased in Nrf2tKOmdx in comparison to mdx mice. In conclusion, the lack of transcriptionally active Nrf2 influences moderately muscle pathology in acute CTX-induced muscle injury and chronic DMD mouse model, without affecting muscle functionality. Hence, in general, we demonstrated that the deficiency of Nrf2 transcriptional activity has no profound impact on muscle pathology in various models of muscle injury.


1997 ◽  
Vol 12 (8) ◽  
pp. 1560-1563 ◽  
Author(s):  
S. Wang ◽  
R. Hirschberg

2007 ◽  
Vol 9 (6) ◽  
pp. 464-468 ◽  
Author(s):  
Marc R. Hammerman ◽  
Steven B. Miller

1990 ◽  
Vol 258 (6) ◽  
pp. F1554-F1560 ◽  
Author(s):  
N. Rossi ◽  
V. Ellis ◽  
T. Kontry ◽  
S. Gunther ◽  
P. Churchill ◽  
...  

It has been proposed that adenosine mediates the renal hemodynamic changes in acute renal failure (ARF) and that these changes are pathogenic in reducing glomerular filtration rate. Consistently, adenosine-receptor antagonists such as theophylline have been shown to have protective effects in several experimental models of ARF. The present experiments were designed to explore the potential role of adenosine in HgCl2-induced ARF in rats. In isolated perfused rat kidneys, HgCl2 increased adenosine production and induced a concentration-dependent vasoconstriction. However, the vasoconstriction was unrelated to adenosine production and was not antagonized by theophylline. During the initiation phase of HgCl2-induced ARF in intact rats (first 4 h after injection), theophylline failed to reverse the reduction in inulin clearance, and this failure could not be attributed to a loss of vascular responsiveness to adenosine, since N6-cyclohexyladenosine, a receptor agonist, produced a further reduction in inulin clearance. Furthermore, theophylline actually had deleterious effects during the maintenance phase of HgCl2-induced ARF in intact unanesthetized rats, as evidenced by higher mean serum creatinine values in theophylline-injected rather than in saline-injected rats, on both the second and third days after HgCl2 injection. Therefore HgCl2 acutely increases renal adenosine production, but increased adenosine does not mediate acute HgCl2-induced renal vasoconstriction, and adenosine-receptor antagonism does not have protective effects during the initiation or the maintenance phases of HgCl2-induced ARF in rats. These results provide no support for the hypothesis that increased adenosine mediates the hemodynamic changes in HgCl2-induced ARF.


Renal Failure ◽  
2007 ◽  
Vol 29 (3) ◽  
pp. 379-386 ◽  
Author(s):  
Alessio Sturiale ◽  
Susanna Campo ◽  
Eleonora Crascì ◽  
Carmela Aloisi ◽  
Michele Buemi

2004 ◽  
Vol 19 (1) ◽  
pp. 93-96 ◽  
Author(s):  
Rachita Nanda ◽  
Pramila K. Mishra ◽  
U. K. Das ◽  
S. B. Rout ◽  
P. C. Mohapatra ◽  
...  

2002 ◽  
Vol 36 (9) ◽  
pp. 1466-1470 ◽  
Author(s):  
Donald F Brophy

OBJECTIVE: To examine the role of N-acetylcysteine (NAC) in the prevention of radiocontrast—induced nephropathy (RIN). DATA SOURCES: A literature search of MEDLINE (1966–December 2001) was performed using the following search terms: N-acetylcysteine, nephropathy, acute renal failure, and radiocontrast. STUDY SELECTION: Pertinent English-language animal and human studies were reviewed. DATA SYNTHESIS: Few small animal trials have demonstrated that NAC significantly prevents the development or reduces the severity of acute renal failure. Two human studies demonstrated NAC significantly reduces the occurrence of RIN. CONCLUSIONS: NAC may reduce the occurrence of RIN in high-risk patients. Further large-scale studies are needed to corroborate findings from earlier trials.


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