Mechanobiology of Adipose Tissue Remodeling.

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)

Adipose tissue is a highly plastic organ whose remodeling dynamics are central to whole-body metabolic health. Expansion of white adipose tissue occurs through either hyperplasia, which preserves tissue function, or hypertrophy, which causes local hypoxia, inflammation, and pathological extracellular matrix (ECM) accumulation. Under hypertrophic conditions, the ECM stiffens and transitions from a supportive scaffold to a fibrotic barrier that limits expansion and perpetuates metabolic dysfunction. Understanding how mechanical cues regulate adipose tissue remodeling is, therefore, essential for identifying new therapeutic strategies. Two mechanosensitive cell populations, adipose stem cells (ASC) and mature adipocytes, are central to this process. ASC interpret ECM stiffness and compositional changes, which determine lineage outcomes. Soft and flexible matrices favor adipogenesis, whereas stiff matrices drive fibroblast-like activation and matrix deposition. Adipocytes, though differentiated, retain mechanosensitive signaling capabilities that shape their function. Under chronic mechanical stresses, cytoskeletal remodeling pathways lead to changes in gene expression and partial dedifferentiation toward a fibroblast-like phenotype. Reciprocal signaling between ASC and adipocytes amplifies these processes, establishing feedback loops that reinforce either healthy or pathological r

Evidence level

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

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