Tatiana V. Kudryashova

This study identifies LDHA-lactate-induced over-lactylation and TOP1 accumulation as drivers of PASMC hyper-proliferation and PAH, with TOP1 inhibition reversing these effects.

The paper shows MST1/2 promotes hyper-proliferation and apoptosis resistance in PAH pulmonary vascular cells by up-regulating CDC20.

This study shows PAI-1 deficiency in PASMC promotes pulmonary vascular remodeling and hypertension by enhancing uPA activity, leading to cell proliferation and reduced apoptosis.

This study shows TSC2 deficiency in pulmonary vascular smooth muscle cells leads to ECM remodeling, hyper-proliferation, and pulmonary hypertension, which can be reversed by restoring TSC2 function.