Northwestern University Feinberg School of Medicine
Faculty Profiles
Tomoko  Hayashida, MD, PhD

Tomoko Hayashida, MD, PhD

Research Associate Professor of Pediatrics (Kidney Diseases)

Focus of Work

Bio

Chronic kidney disease (CKD) affects approximately 20% of US population. While primary causes for CKD varies from genetic disorder to metabolic problems, CKD complies with two essential features; injury to podocyte, which is the primary barrier for filtration units of kidney, and progressive scarring of kidney that 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 ...[Read full text]
Chronic kidney disease (CKD) affects approximately 20% of US population. While primary causes for CKD varies from genetic disorder to metabolic problems, CKD complies with two essential features; injury to podocyte, which is the primary barrier for filtration units of kidney, and progressive scarring of kidney that 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.
We recently found that a signaling molecule, gamma isoform of PI3K, is increased in diseased podocytes in patients’ samples with progressive form of CKD, but not in those with minimal change disorder and inhibiting this molecule prevents podocyte injury in animal models, suggesting that this molecule is a novel therapeutic target.
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. TGF-ß is a pleiotropic cytokine and exerts such function via a receptor and a transcription factor, Smad, regulated by the ligand-binding activation of the receptor. We recently reported HIF, hypoxia inducible factor, modulates fibrogenic functions of TGF-ß, suggesting viscous cycle, contributing to progression of CKD.
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.[Shorten text]

Keywords


Education and Certification

  • MD: Keio University Medical School (1988)
  • PhD: Keio University Medical School, Medical Science (2004)

Contact

312-503-0089

Searle Building Room 4-491
320 E Superior
Chicago IL 60611