Iekuni Ichikawa
Last active: 1/25/2012


Our research is geared to finding the therapeutic target for preventing and reversign the progressive deterioration that occurs in many kidney disesases of children.  Children acquire kidney disease after birth, just as adults, but also congenitally. 

Thus, our research has two major foci, i.e., the cause of congenital kidney diseases, and that of acquired kidney diseases unique to the pediatric population.  By employing state-of-the-art technologies of genetic manipulation in the mouse and genetic analysis in humans, we discovered that the rennin-angiotensin system (RAS) has an important role in the development of both congenital and acquired forms of kidney diseases in children.  In the process of these studies, we have developed a unique mouse model of progressive kidney disease that closely phenocopies the human counterpart, so that we are now able to take full advantage of using mouse recombinant technology to delineate other factors and mechanisms that are key to kidney disease.  We have also found the cause of concurrent abnormalities of the kidney that frequently accompany congenital urinary tract anomalies, which led us to coin a new disease entity as congenital anomalies of the kidney and urinary tract (CAKUT.)  (This was intended to remind that children with urinary tract anomalies, which are readily demonstrable by ultrasonography, may likely have kidney anomalies concurrently that are not demonstrable by imaging analysis; yet have the potential to progress to kidney failure.)  Our laboratory is studying the mechanism underlying this concurrency of anomalies in the kidney and urinary tract that occur congenitally. 


The following timeline graph is generated from all co-authored publications.

Featured publications are shown below:

  1. Podocyte injury damages other podocytes. Matsusaka T, Sandgren E, Shintani A, Kon V, Pastan I, Fogo AB, Ichikawa I (2011) J Am Soc Nephrol 22(7): 1275-85
    › Primary publication · 21719786 (PubMed) · PMC3137575 (PubMed Central)
  2. Induction of podocyte-derived VEGF ameliorates podocyte injury and subsequent abnormal glomerular development caused by puromycin aminonucleoside. Ma J, Matsusaka T, Yang HC, Zhong J, Takagi N, Fogo AB, Kon V, Ichikawa I (2011) Pediatr Res 70(1): 83-9
    › Primary publication · 21451433 (PubMed) · PMC3113658 (PubMed Central)
  3. Glomerular sclerosis is prevented during urinary tract obstruction due to podocyte protection. Matsusaka T, Kobayashi K, Kon V, Pastan I, Fogo AB, Ichikawa I (2011) Am J Physiol Renal Physiol 300(3): F792-800
    › Primary publication · 21177778 (PubMed) · PMC3064125 (PubMed Central)
  4. Angiotensin receptor blocker protection against podocyte-induced sclerosis is podocyte angiotensin II type 1 receptor-independent. Matsusaka T, Asano T, Niimura F, Kinomura M, Shimizu A, Shintani A, Pastan I, Fogo AB, Ichikawa I (2010) Hypertension 55(4): 967-73
    › Primary publication · 20142565 (PubMed) · PMC2887658 (PubMed Central)
  5. Genetic podocyte lineage reveals progressive podocytopenia with parietal cell hyperplasia in a murine model of cellular/collapsing focal segmental glomerulosclerosis. Suzuki T, Matsusaka T, Nakayama M, Asano T, Watanabe T, Ichikawa I, Nagata M (2009) Am J Pathol 174(5): 1675-82
    › Primary publication · 19359523 (PubMed) · PMC2671256 (PubMed Central)
  6. Megalin contributes to the early injury of proximal tubule cells during nonselective proteinuria. Motoyoshi Y, Matsusaka T, Saito A, Pastan I, Willnow TE, Mizutani S, Ichikawa I (2008) Kidney Int 74(10): 1262-9
    › Primary publication · 18769366 (PubMed) · PMC2615689 (PubMed Central)
  7. Bmp in podocytes is essential for normal glomerular capillary formation. Ueda H, Miyazaki Y, Matsusaka T, Utsunomiya Y, Kawamura T, Hosoya T, Ichikawa I (2008) J Am Soc Nephrol 19(4): 685-94
    › Primary publication · 18272846 (PubMed) · PMC2390961 (PubMed Central)
  8. Effects of podocyte injury on glomerular development. Ma J, Rossini M, Yang HC, Zuo Y, Fogo AB, Ichikawa I (2007) Pediatr Res 62(4): 417-21
    › Primary publication · 17667850 (PubMed)
  9. HIV-1 genes vpr and nef synergistically damage podocytes, leading to glomerulosclerosis. Zuo Y, Matsusaka T, Zhong J, Ma J, Ma LJ, Hanna Z, Jolicoeur P, Fogo AB, Ichikawa I (2006) J Am Soc Nephrol 17(10): 2832-43
    › Primary publication · 16988066 (PubMed)
  10. Inhibition of endogenous BMP in the glomerulus leads to mesangial matrix expansion. Miyazaki Y, Ueda H, Yokoo T, Utsunomiya Y, Kawamura T, Matsusaka T, Ichikawa I, Hosoya T (2006) Biochem Biophys Res Commun 340(2): 681-8
    › Primary publication · 16389070 (PubMed)
  11. Rapid downregulation of beta-actin-based CAG promoter and filamentous actin in injured podocytes. Asano T, Matsusaka T, Mizutani S, Ichikawa I (2005) J Med Dent Sci 52(2): 129-34
    › Primary publication · 16189885 (PubMed)
  12. Expression of HIV-1 genes in podocytes alone can lead to the full spectrum of HIV-1-associated nephropathy. Zhong J, Zuo Y, Ma J, Fogo AB, Jolicoeur P, Ichikawa I, Matsusaka T (2005) Kidney Int 68(3): 1048-60
    › Primary publication · 16105035 (PubMed)
  13. Permanent genetic tagging of podocytes: fate of injured podocytes in a mouse model of glomerular sclerosis. Asano T, Niimura F, Pastan I, Fogo AB, Ichikawa I, Matsusaka T (2005) J Am Soc Nephrol 16(8): 2257-62
    › Primary publication · 15987751 (PubMed)
  14. Podocyte damage damages podocytes: autonomous vicious cycle that drives local spread of glomerular sclerosis. Ichikawa I, Ma J, Motojima M, Matsusaka T (2005) Curr Opin Nephrol Hypertens 14(3): 205-10
    › Primary publication · 15821411 (PubMed)
  15. Genetic engineering of glomerular sclerosis in the mouse via control of onset and severity of podocyte-specific injury. Matsusaka T, Xin J, Niwa S, Kobayashi K, Akatsuka A, Hashizume H, Wang QC, Pastan I, Fogo AB, Ichikawa I (2005) J Am Soc Nephrol 16(4): 1013-23
    › Primary publication · 15758046 (PubMed)
  16. Suppression of cyclosporine a nephrotoxicity in vivo by transforming growth factor beta receptor-immunoglobulin G chimeric protein. Xin J, Homma T, Matsusaka T, Ma J, Isaka Y, Imai E, Ichikawa I (2004) Transplantation 77(9): 1433-42
    › Primary publication · 15167603 (PubMed)
  17. Local actions of endogenous angiotensin II in injured glomeruli. Ma J, Matsusaka T, Yang H, Kawachi H, Shimizu F, Isaka Y, Imai E, Kon V, Ichikawa I (2004) J Am Soc Nephrol 15(5): 1268-76
    › Primary publication · 15100367 (PubMed)
  18. Ontogeny of congenital anomalies of the kidney and urinary tract, CAKUT. Miyazaki Y, Ichikawa I (2003) Pediatr Int 45(5): 598-604
    › Primary publication · 14521544 (PubMed)
  19. Evidence that bone morphogenetic protein 4 has multiple biological functions during kidney and urinary tract development. Miyazaki Y, Oshima K, Fogo A, Ichikawa I (2003) Kidney Int 63(3): 835-44
    › Primary publication · 12631064 (PubMed)
  20. Absence of angiotensin II type 1 receptor in bone marrow-derived cells is detrimental in the evolution of renal fibrosis. Nishida M, Fujinaka H, Matsusaka T, Price J, Kon V, Fogo AB, Davidson JM, Linton MF, Fazio S, Homma T, Yoshida H, Ichikawa I (2002) J Clin Invest 110(12): 1859-68
    › Primary publication · 12488436 (PubMed) · PMC151648 (PubMed Central)
  21. Paradigm shift from classic anatomic theories to contemporary cell biological views of CAKUT. Ichikawa I, Kuwayama F, Pope JC, Stephens FD, Miyazaki Y (2002) Kidney Int 61(3): 889-98
    › Primary publication · 11849443 (PubMed)
  22. The renin angiotensin system and kidney development. Matsusaka T, Miyazaki Y, Ichikawa I (2002) Annu Rev Physiol : 551-61
    › Primary publication · 11826279 (PubMed)