Ibrahim Qamhieh
Research Mentor(s): Abdulsalam Soofi
Mentor Department: Nephrology
Authors: Abdul Soofi, Pallavi Fisher , Ibrahim Qamhieh
Session: Session 4 (1:00pm – 1:50pm)
Presentation Type: Poster 67
Abstract
Iron homeostasis is crucial for cellular function, yet its dysregulation can contribute to kidney pathology. Ferroportin (FPN) is the primary iron exporter in renal proximal tubules, responsible for iron resorption and systemic regulation. This study investigates the consequences of renal-specific FPN deletion on iron metabolism and kidney injury recovery. Using a mouse model with proximal tubule-specific knockout of FPN, we observed significant intracellular iron accumulation without baseline functional impairment. However, upon acute kidney injury (AKI) induction, FPN-deficient kidneys exhibited exacerbated damage, increased ferroptosis, and impaired recovery, leading to chronic fibrosis. These findings highlight the critical role of iron export in renal health and suggest that iron dysregulation may contribute to chronic kidney disease (CKD) progression. Understanding iron handling mechanisms in the kidney may provide new therapeutic strategies to mitigate AKI-induced renal damage.
