Evidence map›Paper›PMID 39497227›Full record

ArticleJournal of animal science and biotechnology2024

The assembly and activation of the PANoptosome promote porcine granulosa cell programmed cell death during follicular atresia.

Hao Wu, Yingxue Han, Jikang Liu, Rong Zhao, Shizhen Dai, Yajun Guo, Nan Li, Feng Yang, Shenming Zeng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of animal science and biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. METTL3 inhibition attenuates AFBJournal of animal science and biotechnology · 2026
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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

9 authors.

Hao Wu *National Engineering Laboratory for Animal Breeding, Key Laboratory of Animal Genetics and Breeding of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing, 100193, China.
Yingxue Han *National Engineering Laboratory for Animal Breeding, Key Laboratory of Animal Genetics and Breeding of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing, 100193, China.
Jikang LiuNational Engineering Laboratory for Animal Breeding, Key Laboratory of Animal Genetics and Breeding of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing, 100193, China.
Rong ZhaoNational Engineering Laboratory for Animal Breeding, Key Laboratory of Animal Genetics and Breeding of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing, 100193, China.
Shizhen DaiNational Engineering Laboratory for Animal Breeding, Key Laboratory of Animal Genetics and Breeding of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing, 100193, China.
Yajun GuoNational Engineering Laboratory for Animal Breeding, Key Laboratory of Animal Genetics and Breeding of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing, 100193, China.
Nan LiDepartment of Clinical Sciences, College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China.
Feng YangCollege of Animal Science and Technology, Henan Agricultural University, Zhengzhou, 450046, China. chinafy6868@163.com.
Shenming ZengNational Engineering Laboratory for Animal Breeding, Key Laboratory of Animal Genetics and Breeding of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing, 100193, China. zengsm@cau.edu.cn.ORCID http://orcid.org/0000-0003-2188-6122

Funding

National Natural Science Foundation of China 2022YFD1300405National Natural Science Foundation of China 32202671Open project of State Key Laboratory of Animal Biotech Breeding 2024SKLAB6-5
6 · The paper itself

Abstract

backgroundFollicular atresia significantly impairs female fertility and hastens reproductive senescence. Apoptosis of granulosa cells is the primary cause of follicular atresia. Pyroptosis and necroptosis, as additional forms of programmed cell death, have been reported in mammalian cells. However, the understanding of pyroptosis and necroptosis pathways in granulosa cells during follicular atresia remains unclear. This study explored the effects of programmed cell death in granulosa cells on follicular atresia and the underlying mechanisms.

resultsThe results revealed that granulosa cells undergo programmed cell death including apoptosis, pyroptosis, and necroptosis during follicular atresia. For the first time, we identified the formation of a PANoptosome complex in porcine granulosa cells. This complex was initially identified as being composed of ZBP1, RIPK3, and RIPK1, and is recruited through the RHIM domain. Additionally, we demonstrated that caspase-6 is activated and cleaved, interacting with RIPK3 as a component of the PANoptosome. Heat stress may exacerbate the activation of the PANoptosome, leading to programmed cell death in granulosa cells.

conclusionsOur data identified the formation of a PANoptosome complex that promoted programmed cell death in granulosa cells during the process of follicular atresia. These findings provide new insights into the molecular mechanisms underlying follicular atresia.

Indexed as

Follicular atresiaGranulosa cellsPANoptosomeProgrammed cell death

Identifiers

PMID39497227
PMCPMC11536665

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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.