L. J. Jimenez-Borreguero

This study shows that activating HIF2 causes vascular remodeling, inflammation, and coronary issues similar to Kawasaki disease, using a new mouse model and human tissue analysis.

This study identifies miR-721 as a Th17-derived miRNA that drives autoimmune myocarditis by repressing PPARγ, offering a therapeutic target for treatment.

This paper shows that MKK6 deficiency leads to cardiac dysfunction through hyperactivation of the MKK3-p38γ/δ-mTOR pathway, causing hypertrophy and fibrosis, and highlights potential cardiotoxicity of p38 inhibitors.

The paper investigates the effects of HIF1 deletion in cardiac progenitors, finding that it leads to impaired glycolysis and activation of an amino acid metabolic program without affecting heart development or function.

This study investigates the effects of HIF1α deletion in cardiac progenitors during heart development, finding that HIF1 is dispensable for cardiac growth and reveals metabolic reprogramming toward amino acid utilization.

This study shows that deleting NOTCH-RBPJ in the myocardium does not impair heart development or function, but deleting it in both myocardial and endocardial progenitors causes cardiac defects.