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首页> 外文期刊>Cell and Tissue Research >TGF-β1 → SMAD/p53/USF2 → PAI-1 transcriptional axis in ureteral obstruction-induced renal fibrosis.
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TGF-β1 → SMAD/p53/USF2 → PAI-1 transcriptional axis in ureteral obstruction-induced renal fibrosis.

机译：TGF-β1→SMAD / p53 / USF2→PAI-1转录轴在输尿管梗阻引起的肾纤维化中的作用。

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摘要

Chronic kidney disease constitutes an increasing medical burden affecting 26 million people in the United States alone. Diabetes, hypertension, ischemia, acute injury, and urological obstruction contribute to renal fibrosis, a common pathological hallmark of chronic kidney disease. Regardless of etiology, elevated TGF-β1 levels are causatively linked to the activation of profibrotic signaling pathways initiated by angiotensin, glucose, and oxidative stress. Unilateral ureteral obstruction (UUO) is a useful and accessible model to identify mechanisms underlying the progression of renal fibrosis. Plasminogen activator inhibitor-1 (PAI-1), a major effector and downstream target of TGF-β1 in the progression of several clinically important fibrotic disorders, is highly up-regulated in UUO and causatively linked to disease severity. SMAD and non-SMAD pathways (pp60(c-src), epidermal growth factor receptor [EGFR], mitogen-activated protein kinase, p53) are required for PAI-1 induction by TGF-β1. SMAD2/3, pp60(c-src), EGFR, and p53 activation are each increased in the obstructed kidney. This review summarizes the molecular basis and translational significance of TGF-β1-stimulated PAI-1 expression in the progression of kidney disease induced by ureteral obstruction. Mechanisms discussed here appear to be operative in other renal fibrotic disorders and are relevant to the global issue of tissue fibrosis, regardless of organ site.
机译：慢性肾脏病构成了越来越大的医疗负担，仅在美国就影响了2600万人。糖尿病，高血压，局部缺血，急性损伤和泌尿系统阻塞导致肾脏纤维化，这是慢性肾脏疾病的常见病理标志。不论病因如何，TGF-β1水平的升高均与血管紧张素，葡萄糖和氧化应激引发的纤维化信号通路的激活相关。单侧输尿管梗阻（UUO）是一种有用且可访问的模型，可用于识别潜在的肾纤维化进展机制。纤溶酶原激活物抑制剂1（PAI-1）是几种临床上重要的纤维化疾病进展中TGF-β1的主要效应物和下游靶标，在UUO中高度上调，并与疾病的严重程度有因果关系。 TGF-β1诱导PAI-1时需要SMAD和非SMAD途径（pp60（c-src），表皮生长因子受体[EGFR]，促分裂原活化蛋白激酶，p53）。在阻塞性肾脏中，SMAD2 / 3，pp60（c-src），EGFR和p53激活均增加。综述了TGF-β1刺激的PAI-1表达在输尿管梗阻所致肾脏疾病进展中的分子基础和翻译意义。此处讨论的机制似乎在其他肾纤维化疾病中有效，并且与器官纤维化的全球问题有关，而与器官部位无关。

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