Figure 7.Schematic illustration of the lipodystrophy and insulin resistance exhibited by patients with WS. The genomic repair defect caused by pathogenic variants of the WRN gene leads to chronic inflammation and cellular senescence, resulting in inhibition of adipogenesis and dysfunction of adipocytes, leading to subcutaneous fat mass and quality loss, which in turn leads to subcutaneous fat atrophy and insulin resistance in patients with WS. WS: Werner syndrome; SVF: stromal vascular fraction; SASP: senescence-associated secretory phenotypes.
