Fibrosis and renal aging

Abstract

Glomerulosclerosis and interstitial fibrosis increase in the aging kidney, and glomerular filtration rate (GFR) decreases with increasing age. Decreases in stem cell number and function contribute to renal aging. High-dose angiotensin receptor blocker (ARB) not only slows the progression of glomerular and vascular sclerosis in aging but can also induce regression of these processes independently of its hemodynamic actions. By using new interventions, such as peroxisome proliferator activator receptor gamma (PPARγ) agonist, we can manipulate the process of renal aging by regulating stem cells and other mechanisms.

Keywords: PPARγ; aging; angiotensin; glomerulosclerosis; stem cells.

Figure 1

Young bone marrow reduces renal injury in aging. The bone marrow from young mice or old mice was transplanted into aged mice. Six months later, there was more interstitial fibrosis and glomerular mesangial expansion in old-to-old (O2O) compared with young-to-old (Y2O) bone marrow transplant mice ((a) periodic acid–Schiff staining, × 200). Young bone marrow resulted in significantly less glomerular collagen IV deposition than old bone marrow ((b) × 400). Klotho, the antiaging protein, is mainly expressed in distal tubules. Its level was preserved in young bone marrow–transplanted mice, and was decreased in old bone marrow–transplanted mice (c).