Nogueira António, Pires Maria João, Oliveira Paula Alexandra
Center for the Research and Technology of Agro-Environmental and Biological Sciences, University of Trás-os-Montes and Alto Douro, Vila Real, Portugal.
Department of Therapeutic and Diagnostic Technologies, Polytechnic Institute of Bragança, Bragança, Portugal.
In Vivo. 2017 Jan 2;31(1):1-22. doi: 10.21873/invivo.11019.
Chronic kidney disease (CKD) is a long-term condition in which the kidneys do not work correctly. It has a high prevalence and represents a serious hazard to human health and estimated to affects hundreds of millions of people. Diabetes and hypertension are the two principal causes of CKD. The progression of CKD is characterized by the loss of renal cells and their replacement by extracellular matrix (ECM), independently of the associated disease. Thus, one of the consequences of CKD is glomerulosclerosis and tubulointerstitial fibrosis caused by an imbalance between excessive synthesis and reduced breakdown of the ECM. There are many molecules and cells that are associated with progression of renal fibrosis e.g. angiotensin II (Ang II). Therefore, in order to understand the biopathology of renal fibrosis and for the evaluation of new treatments, the use of animal models is crucial such as: surgical, chemical and physical models, spontaneous models, genetic models and in vitro models. However, there are currently no effective treatments for preventing the progression of renal fibrosis. Therefore it is essential to improve our knowledge of the cellular and molecular mechanisms of the progress of renal fibrosis in order to achieve a reversion/elimination of renal fibrosis.
慢性肾脏病（CKD）是一种长期疾病，其中肾脏无法正常工作。它具有高患病率，对人类健康构成严重危害，估计影响数亿人。糖尿病和高血压是CKD的两个主要原因。CKD的进展特征是肾细胞丢失并被细胞外基质（ECM）取代，这与相关疾病无关。因此，CKD的后果之一是由ECM过度合成与降解减少之间的失衡导致的肾小球硬化和肾小管间质纤维化。有许多分子和细胞与肾纤维化的进展相关，例如血管紧张素II（Ang II）。因此，为了理解肾纤维化的生物病理学并评估新的治疗方法，使用动物模型至关重要，如手术模型、化学模型和物理模型、自发模型、遗传模型和体外模型。然而，目前尚无有效治疗方法来预防肾纤维化的进展。因此，提高我们对肾纤维化进展的细胞和分子机制的认识，以实现肾纤维化的逆转/消除至关重要。
