ArticleOxidative medicine and cellular longevity2022
Dopamine D2 Receptor Signaling Attenuates Acinar Cell Necroptosis in Acute Pancreatitis through the Cathepsin B/TFAM/ROS Pathway.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Dual-Hit Myopia Mechanism Unveiled by Multi-Omics: Opn1mw Deficiency Primed the Retina for Exaggerated Response to Environmental Defocus.Investigative ophthalmology & visual science · 2026Article
- Cell death and its interaction with mitochondrial dysfunction in pathogenesis of acute pancreatitis: a comprehensive review.Apoptosis : an international journal on programmed cell death · 2026Review
- The Intricate Balance between Life and Death: ROS, Cathepsins, and Their Interplay in Cell Death and Autophagy.International journal of molecular sciences · 2024Review
- Identification of Cathepsin B as a Therapeutic Target for Ferroptosis of Macrophage after Spinal Cord Injury.Aging and disease · 2023Article
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Authors and funding
9 authors at 1 institution in 1 country.
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Abstract
Acute pancreatitis (AP) is an inflammatory disease that is associated with trypsinogen activation, mitochondrial dysfunction, cell death, and inflammation. Dopamine D2 receptor (DRD2) plays an essential role in alleviating AP, while it is unclear whether it is involved in regulating acinar cell necroptosis. Here, we found that DRD2 agonist quinpirole alleviated acinar cell necroptosis via inhibiting cathepsin B (CTSB). Moreover, CTSB inhibition by CA-074Me ameliorated AP severity by reducing necroptosis. Notably, knockdown of TFAM reversed the therapeutic effect of either quinpirole or CA-074Me. We identified a new mechanism that DRD2 signaling inhibited CTSB and promoted the expression of mitochondrial transcription factor A(TFAM), leading to reduction of ROS production in AP, which attenuated acinar cell necroptosis ultimately. Collectively, our findings provide new evidence that DRD2 agonist could be a new potential therapeutic strategy for AP treatment.
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