ArticleNutrients2020
JNK/p66Shc/ITCH Signaling Pathway Mediates Angiotensin II-induced Ferritin Degradation and Labile Iron Pool Increase.
Article in Nutrients, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Ischemic preconditioning modulates iron metabolism, acute inflammatory and neurotrophic responses to anaerobic exercise in untrained individuals: a randomized controlled trial.Scientific reports · 2026Trial
- Lithium exposure causes ferroptosis to induce unexplained miscarriage through non-canonical MBOAT1 pathway.Nature communications · 2025Article
- Itchy E3 Ubiquitin Ligase-Mediated Ubiquitination of Ferritin Light Chain Contributes to Endothelial Ferroptosis in Atherosclerosis.International journal of molecular sciences · 2024Article
- Ferroptosis Signaling in Pancreatic β-Cells: Novel Insights & Therapeutic Targeting.International journal of molecular sciences · 2022Review
- Proteomic changes in various organs of Haemaphysalis longicornis under long-term starvation.PLoS neglected tropical diseases · 2022Article
- JNK/Itch Axis Mediates the Lipopolysaccharide-Induced Ubiquitin-Proteasome-Dependent Degradation of Ferritin Light Chain in Murine Macrophage Cells.Inflammation · 2022Article
- Homocysteine-induced decrease in HUVEC cells' resistance to oxidative stress is mediated by Akt-dependent changes in iron metabolism.European journal of nutrition · 2021Article
- Effect of 8-Day Fasting on Leukocytes Expression of Genes and Proteins Involved in Iron Metabolism in Healthy Men.International journal of molecular sciences · 2021Article
- Effect of Ischemic Preconditioning on Marathon-Induced Changes in Serum Exerkine Levels and Inflammation.Frontiers in physiology · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Angiotensin II (Ang II) induces deleterious changes in cellular iron metabolism and increases the generation of reactive oxygen species. This leads to an impairment of neuronal and vascular function. However, the mechanism underpinning Ang II-induced changes in iron metabolism is not known. We hypothesized that Ang II-induced ferritin degradation and an increase in the labile iron pool are mediated by the c-Jun N-terminal kinase (JNK)/p66Shc/ITCH signaling pathway. We show that Ang II treatment induced ferritin degradation in an endothelial cell lines derived from the bovine stem pulmonary artery (CPAE), human umbilical vein endothelial cells (HUVEC), and HT22 neuronal cells. Ferritin degradation was accompanied by an increase in the labile iron pool, as determined by changes in calcein fluorescence. The JNK inhibitor SP600125 abolished Ang II-induced ferritin degradation. Furthermore, the effect of Ang II on ferritin levels was completely abolished in cells transfected with vectors encoding catalytically inactive variants of JNK1 or JNK2. CPAE cells expressing inactive ITCHor p66Shc (substrates of JNK kinases) were completely resistant to Ang II-induced ferritin degradation. These observations suggest that Ang II-induced ferritin degradation and, hence, elevation of the levels of highly reactive iron, are mediated by the JNK/p66Shc/ITCH signaling pathway.
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