Connor W. Lantz

The paper identifies conserved molecular responses to cardiometabolic stress across different disease models and finds PAI-1 as a key mediator of cardiac remodeling.

This study shows that myeloid Hif1 is essential for neonatal cardiac regeneration via IGF-1 signaling, as its loss impairs regenerative function and increases myocardial scarring.

This study shows H19 upregulation in HLHS impairs mitophagy and increases ischemic vulnerability in immature hearts and cardiomyocytes.

This study shows that microglial metabolic reprogramming in HFpEF drives neuroinflammation and cognitive decline, with HIF-1 signaling as a key mediator.

The paper identifies age-specific secretome differences in macrophages under hypoxia and LPS, showing neonatal macrophages have anti-inflammatory, regenerative properties dependent on HIF-1, while adult macrophages show pro-inflammatory, glycolytic responses.