Golor, K
Addressing this gap, this review offers three integrated contributions: first, it positions ferroptosis as a convergent metabolic executioner across a broader spectrum of kidney diseasesencompassing AKI, DN, renal interstitial fibrosis, systemic lupus erythematosus (SLE) nephritis, autosomal dominant polycystic kidney disease (ADPKD), renal cell carcinoma (RCC), and contrast-induced nephropathy (CIN)while emphasizing cell type-specific vulnerabilities: tubular epithelial cells (susceptible via mitochondrial dysfunction), podocytes (via iron overload), and immune cells (e.g., neutrophils/macrophages in SLE nephritis) exhibit context-dependent ferroptosis regulation, governed by cell type-specific modulators [e.g., Nrf2 in tubules, heme oxygenase-1 (HO-1) in macrophages, and sirtuins in podocytes]
Thalassemia can be caused by a number of genetic mutations with varying degrees of severity
In AD, LTF has been identified as a key predictor of amyloid pathology (Tsatsanis et al., 2021) and also directly affects the amyloidogenic A secretory pathway