# Targeting Ferritin in Vascular Calcification Associated With CKD

> **NIH NIH K08** · UNIVERSITY OF ALABAMA AT BIRMINGHAM · 2020 · $168,264

## Abstract

Abstract
The foremost objective of my career is to become an independent and successful physician-scientist in the field
of cardiovascular complications of chronic kidney disease (CKD). My passion to achieve this objective has
helped me since my training began as a medical student in Hungary. To enrich my experience, knowledge and
skills I pursued a PhD degree and worked relentlessly to establish the beginning of my career in U.S. Continuing
on the same path, I was selected in the ABIM research pathway at UAB, a competitive combined program for
residency, fellowship and research training. To fully achieve the goals of my career with an overall emphasis on
improving the health of patients with kidney diseases, I will need further training and mentorship that will also
serve as a fundamental requisite for successful completion of the following scientific premise:
 Calcification of the vasculature is commonly found in patients with advanced CKD and is associated with
increased morbidity and mortality. There is hence an urgent unmet need to find answers to etiologic and
mechanistic questions in order to introduce novel therapeutics. Advanced CKD often results in phosphate
retention and iron deficiency anemia. Whether such iron deficiency in advanced CKD patients promotes vascular
calcification has not been elucidated. We previously reported that iron and 3H-1,2-Dithiole-3-thione (D3T)
induced expression of intracellular ferritin heavy chain (FtH) mitigates transformation of vascular smooth muscle
cells into osteoblast like cells. Based on our preliminary findings, we hypothesize that derangements in iron
metabolism with subsequent decrements in intracellular FtH expression, accelerate CKD associated vascular
calcification. In support of this concept, we hypothesize that parenteral iron administration may be considered to
correct anemia and to prevent vascular calcification in CKD patients. We will also examine the exciting potential
of D3T (a chemo-preventive agent and FtH stimulant), as a therapeutic/preventive agent against vascular
calcification. In this study, we will utilize novel transgenic mice with conditional deletion of FtH in the vascular
smooth muscle cell compartment to test this hypothesis in a model of CKD and hyperphosphatemia. Additionally,
to fully understand the inhibitory role of FtH, we will utilize an unbiased analysis of gene expression using RNA
seq and examine pathways that are involved in the vascular protective effects of FtH.
 Of equal importance, this proposal will serve as a comprehensive strategy intended to transition me from
trainee to independent investigator. I present a curriculum designed to enhance 1) knowledge base in vascular
biology, bioinformatics and biostatistics, 2) technical repertoire with a focus on translational techniques, 3)
professional development through peer mentoring and gaining skills in laboratory management. This training will
be under the guidance of accomplished and respected mentors in a h...

## Key facts

- **NIH application ID:** 9838252
- **Project number:** 5K08HL140294-03
- **Recipient organization:** UNIVERSITY OF ALABAMA AT BIRMINGHAM
- **Principal Investigator:** Abolfazl Zarjou
- **Activity code:** K08 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $168,264
- **Award type:** 5
- **Project period:** 2017-12-15 → 2022-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9838252

## Citation

> US National Institutes of Health, RePORTER application 9838252, Targeting Ferritin in Vascular Calcification Associated With CKD (5K08HL140294-03). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9838252. Licensed CC0.

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