Mechanical interplay between adipose tissues and disease progression

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)

Over the past two decades, an increasing body of evidence has underscored the significant role of the mechanical properties of biological tissues in maintaining tissue functions and regulating cellular changes, such as proliferation, migration, and differentiation. Throughout disease progression, such as in cancers, bone defects, and cardiac conditions, the mechanical microenvironment of tissues can undergo dramatic changes, exerting profound effects on disease development. Adipose tissues are inherently mechanosensitive and mechanoresponsive, continually exposed to various mechanical stresses in daily life. The hypertrophy and accumulation of adipocytes can lead to obesity, a condition strongly associated with numerous health risks, like diabetes and cancers. In this review, we aim to elucidate the reciprocal mechanical interaction between adipose tissues and disease progression, encompassing cancers, bone defects, and cardiac pathologies. The existing literature suggests that alterations in the mechanical microenvironment during disease advancement may impede adipogenic differentiation, induce adipocyte dedifferentiation, and escalate the secretion of inflammatory cytokines. Conversely, dysregulation of adipose tissues can result in the deposition of extracellular matrix components, stiffening the microenvironment and fostering disease progression in a cyclical fashion. There

Evidence level

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

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