Chronic limb-threatening ischemia (CLTI) is characterized by a distinct adipogenic and fibrotic muscular phenotype compared to mild peripheral artery disease (PAD).
The accumulation of intramuscular adipose tissue (IMAT) is negatively correlated with muscle strength and work output in both human subjects and murine models.
Fibroadipogenic progenitor cells (FAPs) are the cellular source of IMAT in ischemic muscle, and their adipogenic potential is regulated by Pparγ signaling.
Genetic or pharmacological inhibition of IMAT formation significantly improves limb function, offering a potential non-revascularization strategy for PAD patients.
Background
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This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
