ArticleFrontiers in pharmacology2025
Endoplasmic reticulum stress aggravates ferroptosis via PERK/ATF4/HSPA5 pathway in UUO-induced renal fibrosis.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Subcellular regulation of ferroptosis: roles of individual intracellular organelles and cross talk.American journal of physiology. Cell physiology · 2026Review
- Programmed cell death in kidney disease: integrated crosstalk among ferroptosis, pyroptosis, apoptosis, and cuproptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Ferroptosis-Based Peripheral Immune Dysregulation and Diagnostic Signatures in Parkinson's Disease: An RNA Transcriptomic and Single-Cell Immune Sequencing Analysis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Integrated transcriptomic and proteomic analysis reveals isolation and culture associated molecular changes in neonatal porcine pancreatic cell clusters.Molecular biology reports · 2026Article
- α-Hederin Alleviates Endoplasmic Reticulum Stress by Upregulating TRIM38 Expression, Thereby Inhibiting Hepatic Stellate Cell Activation and Liver Fibrosis.Biomedicines · 2026Article
- Intermodulation of endoplasmic reticulum stress and ferroptosis in diabetic nephropathy: molecular mechanisms and therapeutic potentials.Apoptosis : an international journal on programmed cell death · 2025Review
- Enzymatic post-translational modifications of proteins in chronic kidney disease: mechanisms, regulation, and clinical significance.Frontiers in pharmacology · 2025Review
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5 authors.
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Abstract
Renal fibrosis, resulting from the transformation of damaged tubular epithelial cells (TECs), serves as a prevalent pathological condition observed in nearly all forms of advancing chronic kidney disease (CKD). Although crucial in fibrotic diseases, the association between endoplasmic reticulum stress (ERS) and ferroptosis remains incompletely elucidated. Herein, increased levels of heat shock protein family A member 5 (HSPA5), acting as a co-molecular in ERS and ferroptosis, along with EMT-associated alterations, including increased α-smooth muscle actin (α-SMA) and Col1a1 levels and decreased E-cad expression, were observed in fibrotic kidneys of Unilateral Ureteral Obstruction (UUO)-induced mouse models and TGF-β-induced EMT in HK-2 cells. The employment of ferrostatin-1 (Fer-1) improved these alterations and reversed TGF-β-induced EMT
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