Evidence map›Paper›PMID 41981703›Full record

ArticleJournal of animal science and biotechnology2026

RFLNA mitigates heat stress-impaired chondrocyte proliferation and vertebral development through cytoskeletal regulation in pigs.

Xiaoyang Yang, Yuxuan Xie, Yabiao Luo, Yubei Wang, Lixian Yang, Longmiao Zhang, Pengxiang Xue, Chengwan Zha, Meiying Fang

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of animal science and biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Xiaoyang YangState Key Laboratory of Animal Biotech Breeding, National Engineering Laboratory for Animal Breeding, MOA Key Laboratory of Animal Genetics and Breeding, College of Animal Science and Technology, Frontiers Science Center for Molecular Design Breeding, Beijing Key Laboratory for Animal Genetic Improvement, China Agricultural University, Beijing, 100193, China.
Yuxuan XieState Key Laboratory of Animal Biotech Breeding, National Engineering Laboratory for Animal Breeding, MOA Key Laboratory of Animal Genetics and Breeding, College of Animal Science and Technology, Frontiers Science Center for Molecular Design Breeding, Beijing Key Laboratory for Animal Genetic Improvement, China Agricultural University, Beijing, 100193, China.
Yabiao LuoState Key Laboratory of Animal Biotech Breeding, National Engineering Laboratory for Animal Breeding, MOA Key Laboratory of Animal Genetics and Breeding, College of Animal Science and Technology, Frontiers Science Center for Molecular Design Breeding, Beijing Key Laboratory for Animal Genetic Improvement, China Agricultural University, Beijing, 100193, China.
Yubei WangSanya Institute of China Agricultural University, Sanya, 572000, China.
Lixian YangState Key Laboratory of Animal Biotech Breeding, National Engineering Laboratory for Animal Breeding, MOA Key Laboratory of Animal Genetics and Breeding, College of Animal Science and Technology, Frontiers Science Center for Molecular Design Breeding, Beijing Key Laboratory for Animal Genetic Improvement, China Agricultural University, Beijing, 100193, China.
Longmiao ZhangSanya Institute of China Agricultural University, Sanya, 572000, China.
Pengxiang XueState Key Laboratory of Animal Biotech Breeding, National Engineering Laboratory for Animal Breeding, MOA Key Laboratory of Animal Genetics and Breeding, College of Animal Science and Technology, Frontiers Science Center for Molecular Design Breeding, Beijing Key Laboratory for Animal Genetic Improvement, China Agricultural University, Beijing, 100193, China.
Chengwan ZhaState Key Laboratory of Animal Biotech Breeding, National Engineering Laboratory for Animal Breeding, MOA Key Laboratory of Animal Genetics and Breeding, College of Animal Science and Technology, Frontiers Science Center for Molecular Design Breeding, Beijing Key Laboratory for Animal Genetic Improvement, China Agricultural University, Beijing, 100193, China.
Meiying FangState Key Laboratory of Animal Biotech Breeding, National Engineering Laboratory for Animal Breeding, MOA Key Laboratory of Animal Genetics and Breeding, College of Animal Science and Technology, Frontiers Science Center for Molecular Design Breeding, Beijing Key Laboratory for Animal Genetic Improvement, China Agricultural University, Beijing, 100193, China. meiying@cau.edu.cn.

Funding

the Key R&D Program of Shandong Province 2022LZGCQY007the National Key Research and Development Program of China 2023YFF1001001 and 2022YFF1003401the National Natural Science Foundation of China U22A20508the Pinduoduo-China Agricultural University Research Fund PC2024A01003the upgrading program of Shandong Province (2022TSGC1196) and MARA (CARS-36)
6 · The paper itself

Abstract

backgroundGlobal climate change has brought severe challenges to the livestock industry, among which heat stress (HS) acts as a key factor impairing the growth and development of pigs. It has been established that ambient temperature influences body size traits mainly by directly affecting skeletal development, yet the molecular mechanisms by which HS inhibits this process remain largely unclear. The cytoskeleton is critical for mediating cellular morphological adaptation to environmental stimuli, and HS can disturb cellular development by destroying cytoskeletal homeostasis. Previous studies have demonstrated that RFLNA regulates bone development through the cytoskeleton, but whether it alleviates HS-induced chondrocyte damage by modulating the cytoskeleton has not been reported. Therefore, this study was conducted to explore the effects of HS on the proliferation and differentiation of pig thoracic vertebral growth plate chondrocytes (PTVCs), and to clarify the regulatory mechanism by which the regulatory factor RFLNA endows PTVCs with HS resistance.

resultsTranscriptomic profiling of PTVCs cultured under control (37 °C) and HS (41 °C) conditions at multiple differentiation time points revealed that HS suppressed cell proliferation and extracellular matrix synthesis. Differentially expressed genes (DEGs) in the early HS response (6 h and 24 h) were enriched in inflammation and stress-response pathways. In contrast, DEGs from later-phases (48, 96, and 144 h) were linked to cytoskeletal reorganization. Further analysis revealed that RFLNA expression was upregulated both by HS and during chondrocyte differentiation. RFLNA expression was higher in the thoracic vertebrae tissues from large-sized Yorkshire pigs than in those from small-sized Wuzhishan pigs. Spatial expression analysis indicated that RFLNA was predominantly expressed in thoracic and lumbar vertebrae, with subcellular localization to the cytoskeleton. Functional assays demonstrated that RFLNA overexpression under HS conditions promoted PTVC proliferation and adhesion while inhibiting migration, thereby mitigating HS-induced growth suppression. Conversely, RFLNA knockdown exacerbated the detrimental effects of HS.

conclusionsOur findings show RFLNA might be a critical mediator of thermal adaptation and vertebral development, which links cytoskeletal regulation to temperature-related variations in body size. This work provides a theoretical foundation for strategies aimed at enhancing climate resilience in swine.

Indexed as

Body lengthChondrocyte developmentHeat stressPigRFLNA

Identifiers

PMID41981703
PMCPMC13081642

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LicenceCC BY
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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.