通过较大程度地减弱一种特定的细胞蛋白受体的活性，人类肾脏疾病的特定损伤作用可得到缓解。这一研究的科学家来自于北卡罗来纳州立大学和法国的一些大学和医院。
表皮生长因子受体的信号通路
急性肾炎（RPGF）是一种罕见但损害肾功能的疾病，能引起人体肾功能衰竭并导致死亡。这一研究朝着该疾病有效治疗的方向迈出重要的一步。
论文发表在《Nature Medicine》网络版上，研究人员表明，表皮生长因子（EGF）受体是伤口愈合的一种重要成分，它对肾脏特定分子的结合能力阻断后能消除RPGN对小鼠模型的有害作用。
北卡罗来纳州的遗传学系教授兼系主任David Threadgill博士称，EGF受体在细胞表面行使关键通道的功能，特定的分子能结合在这个受体上，并开启了导致炎症的细胞级联反应的通道。当机体需要愈合伤口或切口时，这一结合作用是有益的，但不好的情况是患急性肾炎后炎症反应会过度出现。
EGF受体对急性肾炎的重要性有多大？基因工程修饰的小鼠中EGF受体被特定地敲除掉，急性肾炎就不会发病，也不会损害肾脏组织。研究还表明，抑制EGF受体的特定药物能阻止小鼠肾脏功能衰退。
Threadgill博士称，EGF受体在机体中是很关键的成分，应用范围不仅包括急性肾炎，还包括一些癌症（如结肠癌和乳腺癌）。这一受体必须受到严格地控制，如果短期内抑制该受体，我们能阻止失控的细胞增殖以及炎症反应。因此，这一举措可预防或治疗特定的癌症和疾病。（生物探索译 Pobee）
生物探索推荐英文论文摘要：
The Epidermal Growth Factor Receptor Promotes Glomerular Injury and Renal Failure in Rapidly Progressive Crescentic Glomerulonephritis; the Identification of Possible Therapy
Rapidly progressive glomerulonephritis (RPGN) is a clinical syndrome and a morphological expression of severe glomerular injury. Glomerular injury manifests as a proliferative histological pattern, accumulation of T cells and macrophages, proliferation of intrinsic glomerular cells, accumulation of cells in Bowman's space ("crescents"), and rapid deterioration of renal function. Here we show de novo induction of heparin-binding epidermal growth factor-like growth factor (HB-EGF) in intrinsic glomerular epithelial cells (podocytes) from both mice and humans with RPGN. HB-EGF induction increases phosphorylation of the EGFR/ErbB1 receptor in mice with anti-GBM disease. In HB-EGF-deficient mice, EGFR activation in glomeruli is absent and the course of RPGN is markedly improved. Autocrine HB-EGF induces a phenotypic switch in podocytes in vitro. Conditional deletion of the Egfr gene from podocytes of mice alleviates crescentic glomerulonephritis and the clinical features that accompany RPGN. Finally, pharmacological blockade of EGFR also prevents nephrotic syndrome, infiltration of T cells and macrophages, necrotizing crescentic glomerulonephritis, acute renal failure and death in mice. This approach is effective even when started 4 days after the induction of experimental RPGN, suggesting that targeting the HB-EGF/EGFR pathway could also be clinically beneficial for treatment of human RPGN.
