ArticleTransboundary and emerging diseases2026
Celastrol Suppresses Porcine Deltacoronavirus Replication by Modulating Endoplasmic Reticulum Stress-Associated Ca
Article in Transboundary and emerging diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Celastrol Suppresses Porcine Deltacoronavirus Replication by Modulating Endoplasmic Reticulum Stress-Associated CaTransboundary and emerging diseases · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
Porcine deltacoronavirus (PDCoV) infection causes watery diarrhea and even death in neonatal piglets, leading to substantial economic losses. Meanwhile, emerging evidence indicates the potential risk of PDCoV to threaten human health and public safety. However, the effective vaccines or medicines are deficient. In this study, we evaluated the anti-PDCoV effect of celastrol (CE), a bioactive compound extracted from Tripterygium wilfordii. The results showed that CE significantly inhibited PDCoV replication in a dose-dependent manner and targeted multiple lifecycle stages of the virus. Network pharmacology analysis suggested a potential involvement of endoplasmic reticulum (ER)-related pathways in the antiviral mechanism of CE. Further investigation demonstrated that PDCoV infection induced calcium accumulation, which was restored to the baseline by the treatment of CE. Modulation of cellular calcium using chelating or supplementation approaches also influenced PDCoV replication, indicating an association between calcium homeostasis and viral infection. In addition, PDCoV also induced ER stress and increased the calcium level associated with ER, which was attenuated by CE administration. Pharmacological inhibition of ER stress similarly reduced viral replication and altered calcium distribution. Moreover, the molecular docking analysis further suggested that CE may interact with multiple viral proteins, indicating a potential multitarget antiviral profile. Taken together, these findings demonstrate that CE inhibits PDCoV replication in LLC-PK1 cells and is correlated with the regulation of ER stress-associated calcium homeostasis, providing mechanistic insights into host-virus interactions during PDCoV infection.
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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 Socratic graph.