ArticleCell death & disease2021
HO-1 nuclear accumulation and interaction with NPM1 protect against stress-induced endothelial senescence independent of its enzymatic activity.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Viridicatin from the Antarctic FungusAntioxidants (Basel, Switzerland) · 2026Article
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- Mechanism of ribonucleic acid-binding protein ILF2 in promoting diabetic foot ulcer wound healing via regulating the nucleophosmin 1/NF-κB axis.Burns & trauma · 2026Article
- Nucleophosmin 1 proteins as potential therapeutic targets in non-communicable chronic inflammatory diseases: a review of pathophysiological mechanisms.Frontiers in cell and developmental biology · 2026Review
- Targeting Senescence with Apigenin Improves Chemotherapeutic Efficacy and Ameliorates Age-Related Conditions in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Targeting PTGDS Promotes ferroptosis in peripheral T cell lymphoma through regulating HMOX1-mediated iron metabolism.British journal of cancer · 2025Article
- Pyroptosis for osteoarthritis treatment: insights into cellular and molecular interactions inflammatory.Frontiers in immunology · 2025Review
- Mechanism of heme oxygenase-1 regulation of ferroptosis in vascular dementia.Frontiers in molecular neuroscience · 2025Review
- Cytosolic DNA initiates a vicious circle of aging-related endothelial inflammation and mitochondrial dysfunction via STING: the inhibitory effect of Cilostazol.Acta pharmacologica Sinica · 2024Article
- High Hemin Concentration Induces Escape from Senescence of Normoxic and Hypoxic Colon Cancer Cells.Cancers · 2022Article
- The non-canonical effects of heme oxygenase-1, a classical fighter against oxidative stress.Redox biology · 2021Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heme oxygenase-1 (HO-1) has attracted accumulating attention for its antioxidant enzymatic activity. However, the exact regulatory role of its non-enzymatic activity in the cardiovascular system remains unaddressed. Here, we show that HO-1 was accumulated in the nuclei of stress-induced senescent endothelial cells, and conferred protection against endothelial senescence independent of its enzymatic activity. Overexpression of ΔHO-1, a truncated HO-1 without transmembrane segment (TMS), inhibited H
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