Evidence map›Paper›PMID 42208736›Full record

ArticleVirologica Sinica2026

Induction of mitochondrial fission and mtDNA leakage via the Smad3/Drp1 axis by PEDV infection activates the TLR9/NF-κB/IL-1β inflammatory pathway.

Hangao Xie, Jinlian Guan, Fengjie Tian, Ting Xiong, Haixia Feng, Fei Xu, Ziqing Zhou, Dongsheng He, Dingxiang Liu, Ruiai Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Virologica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Hangao XieCollege of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China; Zhaoqing Branch Centre of Guangdong Laboratory for Lingnan Modern Agricultural Science and Technology, Zhaoqing 526200, China.
Jinlian GuanCollege of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China; Zhaoqing Branch Centre of Guangdong Laboratory for Lingnan Modern Agricultural Science and Technology, Zhaoqing 526200, China.
Fengjie TianCollege of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China; Zhaoqing Branch Centre of Guangdong Laboratory for Lingnan Modern Agricultural Science and Technology, Zhaoqing 526200, China.
Ting XiongCollege of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China; Zhaoqing Branch Centre of Guangdong Laboratory for Lingnan Modern Agricultural Science and Technology, Zhaoqing 526200, China.
Haixia FengCollege of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
Fei XuCollege of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
Ziqing ZhouCollege of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
Dongsheng HeCollege of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China; Zhaoqing Branch Centre of Guangdong Laboratory for Lingnan Modern Agricultural Science and Technology, Zhaoqing 526200, China.
Dingxiang LiuCollege of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China; Zhaoqing Branch Centre of Guangdong Laboratory for Lingnan Modern Agricultural Science and Technology, Zhaoqing 526200, China. Electronic address: dxliu0001@163.com.
Ruiai ChenCollege of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China; Zhaoqing Branch Centre of Guangdong Laboratory for Lingnan Modern Agricultural Science and Technology, Zhaoqing 526200, China. Electronic address: chensa727@vip.126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial homeostasis is intricately linked to the pathogenesis of many viral infections. The maintenance of mitochondrial homeostasis and normal cellular functions relies heavily on the delicate balance of mitochondrial dynamics. However, the precise impact of porcine epidemic diarrhea virus (PEDV) infection on mitochondrial dynamics and subsequent pathological processes is largely unexplored. In this study, through both in vivo and in vitro infections, we have demonstrated that PEDV infection induces mitochondrial fission and leakage of mtDNA by upregulating Drp1 expression, and identified Smad3 as a crucial transcription factor responsible for regulating Drp1 expression. By establishing an inflammatory model using PEDV-infected cells, we have identified Drp1-mediated mtDNA release as an upstream event triggering TLR9/NF-κB pathway activation during PEDV infection. These findings provide novel insights into the relationship between PEDV infection and host inflammatory responses from the perspective of mitochondrial dynamics.

Indexed as

Coronavirus InfectionsDNA, MitochondrialDynaminsInterleukin-1betaMitochondrial DynamicsNF-kappa BPorcine epidemic diarrhea virusSmad3 ProteinSwine DiseasesToll-Like Receptor 9AnimalsInflammationMitochondriaSignal TransductionSwineDNA, MitochondrialDynaminsInterleukin-1betaNF-kappa BSmad3 ProteinToll-Like Receptor 9Inflammatory responsesMitochondrial fissionmtDNA leakagePorcine epidemic diarrhea virus (PEDV)Smad3/Drp1 axis

Identifiers

PMID42208736
PMCPMC13469308

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.