The Proliferation and Adipogenic/Fibrogenic Fate Commitment of FAPs via an Autocrine LAMA2/ITGβ1-FAK Pathway.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Intramuscular fat (IMF) deposition is regulated by fibro/adipogenic progenitors (FAPs), which possess bipotent differentiation capacity toward adipocytes or collagen-producing fibroblasts. Dysregulation of this process leads to excessive fibrosis or insufficient adipogenesis. However, the molecular mechanisms governing FAP proliferation and lineage commitment remain unclear. Here, we identified laminin α2 (LAMA2) as an autocrine extracellular matrix protein enriched in FAPs based on single-nucleus RNA sequencing. Functional analyses demonstrated that LAMA2 promotes FAP proliferation and adipogenic differentiation while inhibiting fibrogenesis. Mechanistically, LAMA2 interacts with integrin β1 (ITGβ1) to activate focal adhesion kinase (FAK) signaling, and elevation of p-FAK at Tyr397 was essential for coordinating cell expansion and adipogenic commitment. Inhibition of FAK abrogated the promotion of LAMA2 on FAP proliferation and differentiation. Our study identifies LAMA2 as a key regulator of FAPs that modulates intramuscular fat deposition and fibrosis, representing a promising target for improving livestock meat quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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