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Article

Functional Validation of ALDOA in Regulating Muscle Cell Fate: Based on In Vitro Proliferation, Apoptosis, and Differentiation Experiments

1
Shandong Provincial Key Laboratory for Livestock Germplasm Innovation & Utilization, College of Animal Science and Technology, Shandong Agricultural University, Tai’an 271018, China
2
Henan Key Laboratory of Farm Animal Breeding and Nutritional Regulation, Henan Pig Breeding Engineering Research Centre, Institute of Animal Husbandry, Henan Academy of Agricultural Sciences, Zhengzhou 450002, China
3
Department of Veterinary Medicine, Shandong Vocational Animal Science and Veterinary College, Weifang 261061, China
*
Authors to whom correspondence should be addressed.
Genes 2025, 16(10), 1186; https://doi.org/10.3390/genes16101186 (registering DOI)
Submission received: 26 September 2025 / Revised: 9 October 2025 / Accepted: 11 October 2025 / Published: 12 October 2025
(This article belongs to the Special Issue Advances in Pig Genetic and Genomic Breeding)

Abstract

Background/Objectives: This study systematically investigated the expression characteristics of the ALDOA gene in skeletal muscle cells and its effects on cell proliferation, apoptosis, and differentiation. Methods: We constructed an ALDOA overexpression vector and transfected it into C2C12 cells and porcine skeletal muscle satellite cells. Results: We found that ALDOA exhibited the highest expression in the longissimus dorsi muscle and was primarily localized in the cell nucleus. Overexpression of ALDOA significantly inhibited cell proliferation, induced G0/G1 phase arrest, and downregulated the expression of proliferation-related genes such as CDK2 and Cyclin D1. Concurrently, ALDOA overexpression markedly promoted apoptosis. Regarding differentiation, although ALDOA expression was upregulated during differentiation, its overexpression significantly suppressed the expression of myogenic differentiation-related genes (such as MYOD, MYOG, MEF2C), suggesting a negative regulatory role in differentiation control. Conclusions: This study reveals the multifaceted regulatory functions of ALDOA in skeletal muscle cells, providing experimental evidence for deepening the understanding of its mechanisms in muscle development and regeneration. This study provides the first functional evidence that ALDOA acts as a multifunctional regulator in skeletal muscle cells, negatively governing cell growth and fate decisions by inhibiting proliferation, promoting apoptosis, and impeding myogenic differentiation, thereby extending its role beyond glycolysis to direct governance of cellular processes. This study reveals for the first time that ALDOA possesses dual functions in muscle cells, regulating both metabolism and transcription.
Keywords: C2C12 cells; skeletal muscle satellite cells; ALDOA gene C2C12 cells; skeletal muscle satellite cells; ALDOA gene

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MDPI and ACS Style

Cao, H.; Wang, J.; Wang, Y.; Huang, J.; Chen, W.; Tang, H.; Chen, J.; Xing, B.; Zeng, Y. Functional Validation of ALDOA in Regulating Muscle Cell Fate: Based on In Vitro Proliferation, Apoptosis, and Differentiation Experiments. Genes 2025, 16, 1186. https://doi.org/10.3390/genes16101186

AMA Style

Cao H, Wang J, Wang Y, Huang J, Chen W, Tang H, Chen J, Xing B, Zeng Y. Functional Validation of ALDOA in Regulating Muscle Cell Fate: Based on In Vitro Proliferation, Apoptosis, and Differentiation Experiments. Genes. 2025; 16(10):1186. https://doi.org/10.3390/genes16101186

Chicago/Turabian Style

Cao, Hongzhen, Jing Wang, Yunzhou Wang, Jingsen Huang, Wei Chen, Hui Tang, Junfeng Chen, Baosong Xing, and Yongqing Zeng. 2025. "Functional Validation of ALDOA in Regulating Muscle Cell Fate: Based on In Vitro Proliferation, Apoptosis, and Differentiation Experiments" Genes 16, no. 10: 1186. https://doi.org/10.3390/genes16101186

APA Style

Cao, H., Wang, J., Wang, Y., Huang, J., Chen, W., Tang, H., Chen, J., Xing, B., & Zeng, Y. (2025). Functional Validation of ALDOA in Regulating Muscle Cell Fate: Based on In Vitro Proliferation, Apoptosis, and Differentiation Experiments. Genes, 16(10), 1186. https://doi.org/10.3390/genes16101186

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