Alfieri Carlo, Kavvadas Panagiotis, Simonini Paola, Ikehata Masami, Dussaule Jean Claude, Chadjichristos Christos E, Rastaldi Maria Pia, Messa Piergiorgio, Chatziantoniou Christos
Institut National de la Santé et de la Recherche Médicale Research Unit S_1155, Bâtiment Recherche, Tenon Hospital, Paris, France Department of Medicine and Medical Specialties, Unit of Nephrology, Dialysis, and Renal Transplant, Fondazione Istituto di Ricerca e Cura a Carattere Scientifico Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
Institut National de la Santé et de la Recherche Médicale Research Unit S_1155, Bâtiment Recherche, Tenon Hospital, Paris, France.
Nephrol Dial Transplant. 2015 Dec;30(12):1965-71. doi: 10.1093/ndt/gfv074. Epub 2015 Mar 31.
The incidence and prevalence of chronic kidney disease represents an important problem for public health. In renal diseases, the main histologic alterations derive from the development of renal fibrosis which results from the loss of the balance between pro- and anti-fibrotic factors. Tyrosine kinase receptors (RTKs) and matricellular proteins (MPs) are nowadays studied as potential modulators of renal injury. RTKs regulate cell cycle, migration, metabolism and cellular differentiation. Discoidin domain receptor-1 (DDR-1) is an RTK that has been extensively studied in cancer, and lung and renal diseases. It modulates inflammatory recruitment, extracellular matrix deposition and fibrosis; in renal diseases, it appears to act independently of the underlying disease. MPs regulate cell-matrix interactions and matrix accumulation, cellular adhesion and migration, and expression of inflammatory cells. Periostin is an MP, mainly studied in bone, heart, lung and cancer. Several studies demonstrated that it mediates cell-matrix interactions, migration of inflammatory cells and development of fibrosis. Recently, it has been reported in several nephropathies. In this review, we discuss the potential pathological roles of DDR-1 and periostin focussing on the kidney in both experimental models and human diseases.
慢性肾脏病的发病率和患病率是一个重要的公共卫生问题。在肾脏疾病中，主要的组织学改变源于肾纤维化的发展，而肾纤维化是由促纤维化和抗纤维化因子之间平衡的丧失所致。酪氨酸激酶受体（RTKs）和基质细胞蛋白（MPs）如今被作为肾损伤的潜在调节因子进行研究。RTKs调节细胞周期、迁移、代谢和细胞分化。盘状结构域受体-1（DDR-1）是一种RTK，已在癌症、肺部和肾脏疾病中得到广泛研究。它调节炎症细胞募集、细胞外基质沉积和纤维化；在肾脏疾病中，它似乎独立于潜在疾病发挥作用。MPs调节细胞与基质的相互作用以及基质积累、细胞黏附和迁移，以及炎症细胞的表达。骨膜蛋白是一种MP，主要在骨骼、心脏、肺部和癌症方面进行研究。多项研究表明，它介导细胞与基质的相互作用、炎症细胞的迁移和纤维化的发展。最近，它已在多种肾病中被报道。在本综述中，我们讨论DDR-1和骨膜蛋白在实验模型和人类疾病中对肾脏的潜在病理作用。
