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Interventions to improve chronic cyclosporine A nephrotoxicity through inhibiting renal cell apoptosis: a systematic review / 中华医学杂志(英文版)
Chinese Medical Journal ; (24): 3767-3774, 2013.
Artículo en Inglés | WPRIM | ID: wpr-236174
ABSTRACT
<p><b>OBJECTIVE</b>To reveal interventions for chronic cyclosporine A nephrotoxicity (CCN) and provide new targets for further studies, we analyzed all relevant studies about interventions in renal cell apoptosis.</p><p><b>DATA SOURCES</b>We collected all relevant studies about interventions for cyclosporine A (CsA)-induced renal cell apoptosis in Medline (1966 to July 2010), Embase (1980 to July 2010) and ISI (1986 to July 2010), evaluated their quality, extracted data following PICOS principles and synthesized the data.</p><p><b>STUDY SELECTION</b>We included all relevant studies about interventions in CsA-induced renal cell apoptosis no limitation of research design and language) and excluded the duplicated articles, meeting abstracts and reviews without specific data.</p><p><b>RESULTS</b>There were three kinds of intervention, include anti-oxidant (sulfated polysaccharides, tea polyphenols, apigenin, curcumin, spirulina, etc), biologics (recombinant human erythropoietin (rhEPO), a murine pan-specific transforming growth factor (TGF)-beta-neutralizing monoclonal antibody1D11, cartilage oligomeric matrix protein (COMP)-angiopoietin-1 and hepatocyte growth factor (HGF) gene), and other drugs (spironolactone, rosiglitazone, pirfenidone and colchicine). These interventions significantly improved the CCN, renal cell apoptosis and renal dysfunction through intervening in four apoptotic pathways in animals or protected renal cells from apoptosis induced by CsA and increased cell survival through respectively four pathways in vitro.</p><p><b>CONCLUSIONS</b>There are three group interventions for CCN. Especially anti-oxidant drugs can significantly improve CCN, renal cell apoptosis and renal dysfunction. Many drugs can improve CCN through intervening in Fas/Fas ligand or mitochondrial pathway with sufficient evidences. Angiotensin II, nitric oxide (NO) and endoplasmic reticulum (ER) pathways will be new targets for CCN.</p>
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Patología / Fisiología / Transducción de Señal / Enfermedad Crónica / Ciclosporina / Apoptosis / Receptor fas / Inmunosupresores / Riñón / Mitocondrias Tipo de estudio: Revisiones Sistemáticas Evaluadas Límite: Animales / Humanos Idioma: Inglés Revista: Chinese Medical Journal Año: 2013 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Patología / Fisiología / Transducción de Señal / Enfermedad Crónica / Ciclosporina / Apoptosis / Receptor fas / Inmunosupresores / Riñón / Mitocondrias Tipo de estudio: Revisiones Sistemáticas Evaluadas Límite: Animales / Humanos Idioma: Inglés Revista: Chinese Medical Journal Año: 2013 Tipo del documento: Artículo