ISSN:0886-022X    

DOI:10.3109/08860229609052803

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

ISSN:0886-022X    

DOI:10.3109/08860229609052804

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

ISSN:0886-022X    

DOI:10.3109/08860229609052805

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

摘要:

Much research has been performed to gain better insight into the regeneration process, responsible for the functional and morphological recovery after acute renal failure (ARF). Many investigators focused on endogenously produced polypeptide growth factors as the major mediators of tubular epithelial cell proliferation. However, arguments contradicting this hypothesis have recently gained more support. Indeed, the early decrease of renal epidermal growth factor (EGF) and insulinlike growth factor-1 (IGF-1) in different experimental models of ARF has been frequently shown at both the mRNA and protein level, while other growth factors could not be shown to increase. Moreover, the inaccessibility of the upregulated receptors for endogenously produced growth factors has encouraged research to seek alternative origins for the signals inducing renal regeneration. The accumulation of mononuclear leukocytes in the renal interstitium is a striking observation in renal failure. Where the interstitial disease, recognized by the persistent interstitial accumulation of leukocytes, is a better predictor of chronic renal failure and developing fibrosis, ARF distinguishes itself by the disappearance of the infiltrate when regeneration is complete. The existence of a regenerative potential provided by the network of inflammatory mononuclear leukocytes is supported by studies on tissue repair in different fields. This review discusses the infiltrating network of mononuclear leukocytes as a major participant in the regeneration process after acute renal failure, including the approach which can be followed to investigate this hypothesis.

ISSN:0886-022X    

DOI:10.3109/08860229609052806

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

摘要:

Kidney repair from injury is a major focus of interest for research, both clinical and basic, in the field of acute renal failure. This is so because very little progress has been made during the past several years to improve mortality in hospitalized patients with acute renal failure despite the unique potential of the kidney for complete structural and functional recovery. Novel therapeutic options have recently emerged from the knowledge of molecular mechanisms of tissue injury after ischemia, including pathways of endothelial-leukocyte interaction and epithelial cell aggregation mediated by integrin molecules. These strategies are promising because they may target early mechanisms of leukocyte infiltration and tubular obstruction. However, it seems clear that additional interventions should address the reparative program that potentially leads to the full restoration of kidney structure and function. Thus, acceleration of repair from acute renal failure is achieved experimentally by growth factors which besides different renal actions seem to have in common the ability to stimulate proliferation of surviving tubular epithelial cells. We direct attention to cellular processes which characterize, and possibly have role in, renal repair from acute tubular injury as potential targets of therapy. In addition to proliferation, they include epithelial differentiation and apoptosis. Further investigation in the biology of repair should set the stage for rational design of targeted therapies which may accelerate the pace of recovery and hopefully decrease mortality in such a dramatic and potentially reversible setting.

ISSN:0886-022X    

DOI:10.3109/08860229609052807

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

摘要:

The mortality of acute renal failure (ARF) remains high because most illnesses associated with ARF also cause loss of muscle mass. The mechanisms causing loss of muscle mass are inhibition of protein synthesis and/or acceleration of protein degradation. Identifying which of these abnormalities is present requires understanding the principles of amino acid and protein turnover. There is evidence that ARF by itself impairs protein synthesis and stimulates protein degradation. The mechanisms causing these defects include abnormal metabolic responses to hormones and stimulation of the ATP-ubiquitin-proteasome-dependent pathway. Understanding these mechanisms could lead to rational therapies.

ISSN:0886-022X    

DOI:10.3109/08860229609052808

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

ISSN:0886-022X    

DOI:10.3109/08860229609052809

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

ISSN:0886-022X    

DOI:10.3109/08860229609052810

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

ISSN:0886-022X    

DOI:10.3109/08860229609052811

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor

ISSN:0886-022X    

DOI:10.3109/08860229609052812

出版商:Taylor&Francis    

年代:1996

数据来源: Taylor