Myogenic IL-6 Mediates Myofiber Type Transition in Porcine Skeletal Muscle Satellite Cells via the STAT3/myh7 Pathway
Myofiber type determines pork quality, with type I fibers conferring superior traits via myosin heavy chain 7 (Myh7). As a crucial myokine, interleukin-6 (IL-6) plays important roles in skeletal muscle development, whether it participates in myh7 transcription and type I myofiber differentiation remains unclear. To address this, we compared Putian (adipose-type) and DLY (lean-type) pigs through in vivo myofiber typing and in vitro satellite cell (SC) cultures, supplemented by ChIP-PCR and dual-luciferase reporter assays to investigate molecular mechanisms. Our results showed that Putian pigs exhibited significantly higher proportions of type I myofibers, myh7 mRNA and Myh7 protein expression, and IL-6 levels than DLY pigs. In vitro, IL-6 treatment promoted SC differentiation toward type I myofibers. Mechanistically, STAT3 bound directly to the myh7 promoter in a phosphorylation-dependent manner to enhance its transcription, as confirmed by ChIP-PCR and dual-luciferase reporter assays. STAT3 was required for IL-6-induced myh7 upregulation, and STAT3 inhibition abrogated this effect. Collectively, these findings demonstrate that muscle-derived IL-6 promotes type I myofiber differentiation by activating STAT3 phosphorylation and myh7 transcription, providing a candidate target for improving pork quality through selective breeding or nutritional intervention.
Authors
- Rui Cao (ORCID: https://orcid.org/0000-0003-4444-7528)
- Ruiyi Lin (ORCID: https://orcid.org/0000-0003-3255-5900)
- Tianfang Xiao (ORCID: https://orcid.org/0000-0001-5116-7642)
- Weimin Lin (ORCID: https://orcid.org/0000-0001-7348-4614)
- Chongfan Du
- Chao Li
- Qiuming Deng
- Hui Wei
Institutions
- Fujian Agriculture and Forestry University (CN)
Publication Details
- Journal
- Veterinary Sciences
- Published
- 2026-09-09
- DOI
- https://doi.org/10.3390/vetsci13090927
- Primary Topic
- Muscle Physiology and Disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00