ArticleCell communication and signaling : CCS2024
Dopamine enhances recovery after traumatic brain injury through ubiquitylation and autophagic degradation of RIPK1.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.
- Neural stem cell transplantation in rodent models of traumatic brain injury: a systematic review and meta-analysis.Frontiers in bioengineering and biotechnology · 2026Pooled it
- Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- USP4 modulates ZBP1 ubiquitination to regulate microglial PANoptosis and functional outcomes following traumatic brain injury.Cell death and differentiation · 2026Article
- Harnessing artificial intelligence to identify Bufalin as a molecular glue degrader of estrogen receptor alpha.Nature communications · 2025Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough the neurotransmitter dopamine (DA) plays a crucial pathophysiologic role after traumatic brain injury (TBI), its function and specific underlying mechanisms of action remain unclear.
methodsAdult male mice underwent controlled cortical impact (CCI). We administered DA intraperitoneally to mice for 14 consecutive days, starting 8 h before CCI. On day 3 after brain injury, cortical lesion volume and brain water content were measured. On days 7-13, behavioral tests were performed.
resultsHerein we report that DA inhibits neural death after injury, which is mediated via the dopamine D1 receptor (DRD1). Our results also showed that DRD1 signaling promotes RIPK1 ubiquitination via the E3 ubiquitin ligase Chip and then degradation through autophagy. Importantly, in vivo data revealed that DRD1 signaling prevented neural death, suppressed neuroinflammation, and restored many TBI-related functional sequelae.
conclusionsThese data reveal a novel mechanism involving dopamine, and suggest that DRD1 activation positively regulates Chip-mediated ubiquitylation of RIPK1-leading to its autophagic degradation.
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