Hutchinson-Gilford Progeria Syndrome (HGPS) is a segmental premature aging 
disease causing patient death by early teenage years from cardiovascular 
dysfunction. Although HGPS does not totally recapitulate normal aging, it does 
harbor many similarities to the normal aging process, with patients also 
developing cardiovascular disease, alopecia, bone and joint abnormalities, and 
adipose changes. It is unsurprising, then, that as physicians and scientists 
have searched for treatments for HGPS, they have targeted many pathways known to 
be involved in normal aging, including inflammation, DNA damage, epigenetic 
changes, and stem cell exhaustion. Although less studied at a mechanistic level, 
severe metabolic problems are observed in HGPS patients. Interestingly, new 
research in animal models of HGPS has demonstrated impressive lifespan 
improvements secondary to metabolic interventions. As such, further 
understanding metabolism, its contribution to HGPS, and its therapeutic 
potential has far-reaching ramifications for this disease still lacking a robust 
treatment strategy.