Ade Adebiyi, PhD

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Associate Professor
Phone: 901-448-1868
Fax: 901-448-7126
Full CV


2004 PhD: National University of Singapore, Singapore

Research Interest

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Our current research focuses primarily on the physiology and pathophysiology of renal hemodynamics. We utilize an integrative approach, including cell and molecular biology, physiology, and pharmacology techniques to investigate regulatory proteins, ion channels, and GPCRs that control renal vascular and glomerular functions. Current projects in the lab include:

  1. Control of renal microcirculation in adults and neonates.
  2. Mechanisms of altered microvascular function in acute kidney injury.
  3. Ca2+ signaling in glomerular mesangial cells.

Research Support


  • 07/01/2014 – 06/30/2019: R01DK101668, "Regulation of neonatal renal hemodynamics"
    Role: Principal Investigator
    Agency: National Institutes of Health (NIDDK)
  • 07/01/2016 – 06/30/2018: 16GRNT30990069, "Myogenic renal autoregulation in neonatal acute kidney injury"
    Role: Principal Investigator
    Agency: American Heart Association (Grant-in-Aid)


  • 04/15/2009 – 03/31/2014: K01HL096411, "Vasoregulation by IP3 receptor coupling to TRPC channels"
    Role: Principal Investigator
    Agency: National Institutes of Health (NHLBI)
  • 07/01/2006 - 06/30/2008: Postdoctoral Research Fellowship, "Regulation of the cerebral artery myogenic response by caveolin-1"
    Role: Principal Investigator
    Agency: American Heart Association

Selected Publications

  1. Soni H, ADEBIYI A. Urotensin II-induced store-operated Ca2+ entry contributes to glomerular mesangial cell proliferation and extracellular matrix protein production under high glucose conditions. Scientific Reports 2017; 7:18049.
  2. Soni H, Peixoto-Neves D, Buddington RK, ADEBIYI A. Adenosine A1 receptor-operated calcium entry in afferent arterioles is dependent on postnatal maturation of TRPC3 channels. American Journal of Physiology. Renal Physiology 2017; 313:F1216-F1222.
  3. Soni H, Peixoto-Neves D, Matthews AT, ADEBIYI A. TRPV4 channels contribute to neonatal renal myogenic response. American Journal of Physiology. Renal Physiology 2017; 313:F1136-F1148.
  4. Soni H, ADEBIYI A. Early polymicrobial sepsis in neonatal pigs increases serum and urinary soluble Fas ligand and decreases kidney function without inducing significant renal apoptosis. Renal Failure 2017; 39:83-91.
  5. Soni H and ADEBIYI A.TRPC6 channel activation promotes neonatal glomerular mesangial cell apoptosis via calcineurin/NFAT and FasL/Fas signaling pathways. Scientific Reports 2016; 6:29041.
  6. Soni H, Buddington RK, ADEBIYI A.Postnatal kidney maturation regulates renal artery myogenic constriction. Journal of Perinatal Medicine 2015; 1:119-122.
  7. ADEBIYI A,Soni H, John TA, Yang F. Lipid rafts are required for signal transduction by angiotensin II receptor type 1 in neonatal glomerular mesangial cells. Experimental Cell Research 2014; 324:92-104.
  8. ADEBIYI A. RGS2 regulates urotensin II-induced intracellular Ca2+elevation and contraction in glomerular mesangial cells. Journal of Cellular Physiology 2014; 229:502-511.
  9. Soni H, ADEBIYI A. Pressor and renal regional hemodynamic effects of urotensin II in neonatal pigs. Journal of Endocrinology 2013; 217:317-26.
  10. ADEBIYI A, Thomas-Gatewood CM, Leo MD, Kidd MW, Neeb ZP, Jaggar JH. An elevation in physical coupling of type 1 inositol 1,4,5-trisphosphate (IP3) receptors to transient receptor potential 3 (TRPC3) channels constricts mesenteric arteries in genetic hypertension. Hypertension2012; 60:1213-9.
  11. ADEBIYI A, Narayanan D, Jaggar JH. Caveolin-1 assembles type 1 inositol 1,4,5-trisphosphate receptors and canonical transient receptor potential 3 channels into a functional signaling complex in arterial smooth muscle cells. Journal of Biological Chemistry2011; 286:4341-8. ** Science Signaling Editor's Choice: Gough NR. Coupled by Caveolin. Science Signaling 2011;4:  
  12. ADEBIYI A, Zhao G, Narayanan D, Thomas-Gatewood CM, Bannister JP, Jaggar JH.  Isoform-selective physical coupling of TRPC3 channels to IP3receptors in smooth muscle cells regulates arterial contractility. Circulation Research 2010; 106:1603-12.