Intramuscular adipose tissue: from progenitor to pathology.

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)

The accumulation of intramuscular adipose tissue (IMAT) is a nearly ubiquitous feature of skeletal muscle pathology, strongly correlating with impaired contractility and metabolic dysfunction across a wide spectrum of clinical conditions, from aging and obesity to genetic myopathies and orthopedic injuries. For decades, a critical question has persisted: is IMAT a passive biomarker of disease progression or an active pathogenic agent? This review synthesizes emerging evidence to address this question by exploring several key areas. We first evaluate the mechanisms by which IMAT impairs muscle function, examining evidence for its dual role as both a physical disruptor and a local source of unbalanced paracrine signals. By integrating findings from human studies with insights from diverse animal models, we also highlight significant translational challenges, particularly the resistance of common rodent models to developing human-like IMAT pathology. Furthermore, we review the cellular origin of IMAT to resident fibro/adipogenic progenitors (FAPs), a highly plastic cell population that supports regeneration in healthy muscle but can differentiate into adipocytes under pathological conditions. We then dissect the complex signaling network that governs this fate switch-specifically the balance between proadipogenic "triggers" and inhibitory "brakes" that becomes dysregulated in dise

Evidence level

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

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