ArticleCell death discovery2023
Defective NCOA4-dependent ferroptosis in senescent fibroblasts retards diabetic wound healing.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
40 citing papers in PubMed, 50 citations in OpenAlex.
- The Iron Lung: Ferroptosis and Iron Regulation in Aging and Lung Diseases.Physiology (Bethesda, Md.) · 2027Review
- CNP-miR146a Promotes NRF2-Related Ferroptosis-Protective Myeloid Programs and Immune-Vascular Regeneration in Diabetic Wounds.Pharmaceutics · 2026Article
- Ferroptosis and aging: Inducing and catalyzing neurodegenerative diseases.Neural regeneration research · 2026Article
- Acid ceramidase modulates the lipid profile and exacerbates sensitivity to ferroptosis in WI-38 replicative senescent cells.Cell death & disease · 2026Article
- Crosstalk between autophagy and ferroptosis in diabetes.Genes & diseases · 2026Review
- HIF-1α attenuates ferroptosis-associated dermal fibroblast senescence via modulation of NF-κB-DPP4 signaling.Journal of translational medicine · 2026Article
- Fatty acid channelling into triglycerides and oxylipins drives ferroptosis resistance during oncogenic BRAF-induced senescence.Cell death and differentiation · 2026Article
- A core-shell microneedle platform for the spatiotemporal codelivery of dual-agent therapeutics precisely orchestrates diabetic wound healing.Journal of nanobiotechnology · 2026Article
- aFGF rescues high glucose-induced senescent fibroblasts and improves diabetic wound healing by regulating SIRT1/STAT3 pathway.Scientific reports · 2026Article
- Senolytic-loaded asymmetric wound dressing for targeted senescent cell clearance in diabetic wound healing.Materials today. Bio · 2026Article
- Aging at the Crossroads of Cuproptosis and Ferroptosis: From Molecular Pathways to Age-Related Pathologies and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Metabolic reprogramming in diabetic complications: mechanisms, pathologies, and molecular evidence from multi-organ studies.Frontiers in immunology · 2026Review
- Deciphering the Iron Metabolism and Ferroptosis in Diabetic Wound Healing.Current diabetes reviews · 2026Review
- Autophagy-Ferroptosis Interplay Network: Redefining Therapeutic Paradigms for Diabetic Wound Healing.Journal of inflammation research · 2026Review
- Glucolipid metabolic disorders and ferroptosis in diabetic ulcers: pathogenic crossroads and therapeutic opportunities.Frontiers in endocrinology · 2026Review
- Acid ceramidase modulates the lipid profile and exacerbates sensitivity to ferroptosis in senescent cells.Research square · 2025Article
- Research progress on the role and mechanisms of ferroptosis in diabetic wound repair.Cell death discovery · 2025Review
- An atlas of ferroptosis-induced secretomes.Cell death and differentiation · 2025Article
- Natural Products as Modulators of Iron Metabolism and Ferroptosis in Diabetes and Its Complications.Nutrients · 2025Review
- YTHDF2 regulates ACSL4-dependent ferroptosis of keratinocytes in diabetic wound healing.Clinical science (London, England : 1979) · 2025Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Cellular senescence describes a state of permanent proliferative arrest in cells. Studies have demonstrated that diabetes promotes the pathological accumulation of senescent cells, which in turn impairs cell movement and proliferation. Historically, senescence has been perceived to be a detrimental consequence of chronic wound healing. However, the underlying mechanism that causes senescent cells to remain in diabetic wounds is yet to be elucidated. Ferroptosis and ferritinophagy observed in diabetes are due to iron metabolism disorders, which are directly associated with the initiation and progression of diabetes. Herein, we reveal that senescent fibroblasts in diabetic wounds are resistant to ferroptosis and that impaired ferritinophagy may be a contributing cause. Further, the expression of NCOA4, a key factor that influences ferritinophagy, is decreased in both diabetic wound tissue and high glucose-induced senescent fibroblasts. Moreover, NCOA4 overexpression could render senescent fibroblasts more vulnerable to ferroptosis. A faster wound healing process was also linked to the induction of ferroptosis. Thus, resistance to ferroptosis impedes the removal of senescent fibroblasts; promoting ferritinophagy could reverse this process, which may have significant implications for the management of diabetic wounds.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.