Tomoko Hayashida

  • 1444 Citations
1992 …2021

Research output per year

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Personal profile

Research Interests

Chronic kidney disease (CKD) affects approximately 20% of US population. Primary causes for CKD varies from genetic disorder to metabolic problems, but many are unknown. Regardless of the primary cause, CKD progresses with two essential phases; injury to podocyte, the primary barrier for filtration units of kidney, and progressive scarring of kidney, which would eventually obliterate the filtration units and lead to loss of kidney function. My research goal is to understand the molecular mechanisms underlining these two features of CKD in order for developing novel therapeutic approaches for CKD. To address the first phase podocyte injury, we are currently working on a molecule called p110g. Our data suggest that a specific inhibitor of this molecule may provent podocyte injury. For the second, scarring phase, my previous works revealed several pathways that modulate functions of a scar-promoting cytokine, TGF-beta. Now, we have identified a molecule called SARA is a critical gate keeper to prevent cells from becoming scar forming cells. Since in most cases patients seek to medical care when the initial injury had already occurred, targeting SARA might be beneficial approach treating CKD.

We recently found that a signaling molecule, gamma isoform of PI3K (p110g), is increased in diseased podocytes in patients’ samples with progressive form of CKD, but not in those with minimal change disorder. Inhibiting this molecule either chemically or genetically prevents podocyte injury in animal models. These data suggest that molecule is a novel therapeutic target. An effort seeking a novel, safer compound that block activity of p110g has been launched. We also are interested in deciphering a process by which kidney scarring is initiated and progresses after podocyte injury has occurred, with particular focus on a scar-promoting cytokine, TGF-ß. In searching a regulatory molecule for TGF-beta pathway, we recently identified a Smad Anchor for Receptor Activation (SARA) is a key mediator maintaining epithelial cell type, hence preventing them becoming fibrogenic. By identifying a mechanism how this molecule regulates cellular phenotype will bring new insight in preventing progression of CKD.

Education/Academic qualification

PhD, Keio University Medical School

… → 2004

MD, Keio University Medical School

… → 1988

Research interests

  • Cell Biology
  • Fibrosis
  • Kidney
  • Molecular Biology
  • Signal Transduction
  • Stem Cells
  • TGF-beta
  • Translational Research

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Grants

  • Research Output

    • 1444 Citations
    • 26 Article
    • 3 Review article
    • 1 Editorial

    Anti-TGF-β antibody, 1D11, ameliorates glomerular fibrosis in mouse models after the onset of proteinuria

    Liang, X., Schnaper, H. W., Matsusaka, T., Pastan, I., Ledbetter, S. & Hayashida, T., May 2016, In : PloS one. 11, 5, e0155534.

    Research output: Contribution to journalArticle

  • 9 Scopus citations

    Hypoxia-inducible factor-1alfa promotes glomerulosclerosis and regulates COL1A2 expression through interactions with Smad3

    Baumann, B., Hayashida, T., Liang, X. & Schnaper, HW., 2016, In : Kidney international. 90, 4, p. 797-808 12 p.

    Research output: Contribution to journalArticle

    Hypoxia-inducible factor-1α promotes glomerulosclerosis and regulates COL1A2 expression through interactions with Smad3

    Baumann, B., Hayashida, T., Liang, X. & Schnaper, H. W., Oct 1 2016, In : Kidney international. 90, 4, p. 797-808 12 p.

    Research output: Contribution to journalArticle

  • 17 Scopus citations

    Hypoxia-inducible factor-2α and TGF-β signaling interact to promote normoxic glomerular fibrogenesis

    Hanna, C., Hubchak, S. C., Liang, X., Rozen-Zvi, B., Schumacker, P. T., Hayashida, T. & Schnaper, H. W., Nov 1 2013, In : American Journal of Physiology - Renal Physiology. 305, 9

    Research output: Contribution to journalArticle

  • 24 Scopus citations
  • 10 Scopus citations