Evidence map›Paper›PMID 41290726›Full record

ArticleNPJ science of food2025

AMP-activated protein kinase-Caspase 6 axis regulation alleviates the combined apoptotic damage caused by deoxynivalenol and fumonisin B1 in mammary glands.

Liguang Cao, Guojin Li, Kai Liu, Wenrui Gao, Yifei Dong, Zifeng Yang, Jianchun Luo, Lin Lei, Xiliang Du, Yuxiang Song and 3 more

Abstract read
In one paragraph

Article in NPJ science of food, 2025. 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

13 authors.

Liguang CaoState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China.
Guojin LiState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China.
Kai LiuState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China.
Wenrui GaoState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China.
Yifei DongState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China.
Zifeng YangState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China.
Jianchun LuoState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China.
Lin LeiState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China.
Xiliang DuState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China.
Yuxiang SongState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China.
Xinwei LiState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China.
Wenwen GaoState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China. jilugaoww@126.com.
Guowen LiuState Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China. liuguowen2008@163.com.

Funding

Chongqing science and Technology Bureau CSTB2023NSCQ-MSX0869National Key Research and Development Programs of China 2023YFD1301003the Science Foundation of Education Bureau of Jilin Province JJKH20231203KJ
6 · The paper itself

Abstract

Deoxynivalenol (DON) and fumonisin B1 (FB1) are prevalent mycotoxins commonly found together in dairy cow feed, posing significant risks to cow health and food safety. This study investigates combined toxic effects of DON and FB1 on bovine mammary epithelial cells (BMECs), and role of AMPK-Caspase 6 axis in mycotoxin-induced apoptosis in BMECs and mouse model. We showed that even subcytotoxic doses of DON, combined with FB1, induced synergistic or additive toxic effects, reducing cell viability, increasing LDH release, and promoting apoptosis. This combination also impaired milk triglyceride synthesis and downregulated genes involved in milk fat and protein production. Silencing Caspase 6 via siRNA, inhibiting with Z-VEID-FMK, or activating AMPK with AICAR alleviated apoptosis. Conversely, overexpressing Caspase 6 diminished AMPK's protective effects. In vivo, inhibiting Caspase 6 alleviated apoptosis in mammary tissues. These findings highlight therapeutic potential of targeting the AMPK-Caspase 6 pathway to mitigate combined toxicity of DON and FB1.

Identifiers

PMID41290726
PMCPMC12669614

What OpenQuestion holds

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Registered trials

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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.