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Eduardo Molina-Jijon, PhD

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Eduardo Molina-Jijon, PhD

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Assistant Professor, Department of Internal Medicine, Division of Nephrology

RUSH Medical College

Assistant Professor, Department of Internal Medicine, Division of Nephrology

Contact Information

Address: 1735 W. Harrison St.
Cohn Building, Suite 436
Chicago, IL 60612
Phone:
(312) 563-1573
Fax:
(312) 563-1056
Email:
Eduardo_MolinaJijon@rush.edu

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- PhD, Cellular and Molecular Physiology, Center for Research and Advanced Studies (Cinvestav), Mexico
- MS, Biochemistry, National Autonomous University of Mexico (UNAM), Mexico
- BS, Chemistry, Pharmacy and Biology, National Autonomous University of Mexico (UNAM), Mexico
Eduardo Molina-Jijon, PhD, is Principal investigator of the Glomerular Disease Therapeutics Laboratory. During his postdoctoral fellowship at Rush University Medical Center, he described the first clear molecular mechanisms to understand the link between proteinuria and initiation of hypercholesterolemia in nephrotic syndrome using a combination of transgenic animal models, especially the critical role of the proprotein convertase subtilisin/kexin type 9 (PCSK9) secreted from the kidney cortical conducting duct cells (Kidney International 2020).

Molina-Jijon has also worked on the role of the Zinc Fingers and Homeoboxes family of transcription factors (ZHX proteins) in podocyte biology, including ZHX2. This work led to the discovery of ZHX2 biological pathways in the context of relapse and worsening of Minimal Change Disease (MCD) and Focal and Segmental Glomerulosclerosis (FSGS) (Kidney International 2020). In addition, as a junior faculty, he has worked on SARS-CoV-2/COVID-19 and Rhinovirus Common Cold cytokine storm model of multi-organ injury. Using mouse models, he uncovered pathways to reduce that injury to vital organs such as kidney, heart, and liver (JCI Insight 2023).

Molina-Jijon’s lab is currently investigating the mechanisms related to the development of glomerular injury and albuminuria in Hodgkin’s Lymphoma - induced nephrotic syndrome including experiments relevant to new forms of therapy using cytokine/soluble proteins depletion and/or their receptor blockage.

Molina-Jijon received his PhD from Mexico, followed by postdoctoral fellowship at RUSH University Medical Center. Most recently, Dr Molina-Jijon submitted a NIH R01 grant application entitled “Hodgkin’s Lymphoma-induced Nephrotic Syndrome” and received a fundable score which is under pending NIDDK council review.
- 2021: Fellow “Building Up a Diverse Workforce for Biomedical Research Study” University of Pittsburg Institute for Clinical Research Education (ICRE).
- 2019: First place in the poster presentation competition during the 5th Annual Mentoring Program Symposium. RUSH University Medical Center. Chicago, IL.
- 2018: Selected as oral presenter for scientific merit and outstanding job for the second symposium on diversity and inclusion. RUSH University Medical Center. Chicago, IL. USA.
- 2018: Travel Grant award from the Department of Internal Medicine. RUSH University Medical Center to attend the American Society of Nephrology (ASN) Kidney week 2018.
- 2017: Winner 2017 Wiley-Blackwell BioFactors Young Investigator Award
- 2016: Member of the National System of Researchers in Mexico (SNI, Level 2).
- 2013: Travel Grant award “The Sixteenth Congress of the International Pediatric Nephrology Association”, Shanghai, China.
- 2011-2016 National Scholarship, Ph. D. in Cellular and Molecular Physiology, Cinvestav, Mexico City, Mexico
- 2009 – 2011 National Scholarship, MS in Biochemistry, National Autonomous University of Mexico (UNAM), Mexico City, Mexico
1. NIH R01DK141612 (pending NIDDK Council Review)
  
  Principal Investigator: Eduardo Molina-Jijon
  
  Title: Hodgkin’s Lymphoma-induced nephrotic syndrome
  
  Brief summary: This proposal will explore mechanisms related to the development of glomerular injury and albuminuria in Hodgkin Lymphoma - induced nephrotic syndrome and includes experiments relevant to new forms of therapy using cytokine/soluble proteins depletion and/or their receptor blockage.

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