ArticleCell death discovery2025
UVB-Induced necroptosis of the skin cells via RIPK3-MLKL activation independent of RIPK1 kinase activity.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- The role of inflammatory cell death in type 1 dominant inflammatory skin diseases.Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG · 2026Review
- Induction of stress granules alleviates programmed cell death induced by lysosomal damage during NK cell cryopreservation.Cell death discovery · 2026Article
- Mitochondrial homeostasis meets novel programmed cell death: crosstalk mechanisms underlying cardiovascular diseases progression.Cell communication and signaling : CCS · 2026Review
- Spatial transcriptomic analysis identifies a necroptosis-prone thyroid follicular cell state in Hashimoto's thyroiditis.Frontiers in immunology · 2026Article
- Exosome-Mediated Rewiring of Oxidative Stress-Inflammation-ECM Remodeling Axis Mitigates UVB-Triggered Skin Photoaging.International journal of nanomedicine · 2026Review
- Notoginsenoside R1 mitigates UVB-induced skin sunburn injury through modulation of NChinese medicine · 2025Article
- Donkey milk-derived exosomes protect against UVB irradiation-induced ferroptosis in skin cells:Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ultraviolet B (UVB) is recognized for inducing inflammation and death of keratinocytes through the activation of death receptors and pattern recognition receptors (PRRs). Receptor-interacting protein kinase 1 (RIPK1) and RIPK3 play pivotal roles in mediating necroptosis, which can be triggered by the activation of specific death receptors and PRRs. In this study, we observed a reduction of RIPK1 protein after UVB exposure which led to activation of Nuclear factor-kappa B (NF-κB) in HaCaT cells. This activation, in turn, promoted the production of IL-1β and TNF-α. However, RIPK1 kinase remained inactive and did not participate in cell death. Interestingly, UVB radiation triggered the activation of RIPK3 independently of RIPK1 kinase activity and subsequently induced phosphorylation of mixed-lineage kinase domain-like protein (MLKL), culminating in necroptosis and inflammation of the skin. At the same time, UVB-induced activation of RIPK3 also played a role in promoting the mitochondrial apoptotic pathway of Keratinocytes. In conclusion, UVB irradiation initiates an inflammatory response via RIPK1 pathway without necessitating its enzymatic activity. Simultaneously, RIPK3 can be activated by UVB exposure independently of RIPK1's activity, resulting in necroptosis and inflammation of the skin.
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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.