Martin Alexander Schwartz

This study identifies PDK4 as a regulator of TGF{beta}-mediated SMC contractility, showing that reducing PDK4 limits atherosclerosis by preserving SMC phenotype.

This study shows that deleting KLF4 in maternal endothelium causes gestational hypertension and features of preeclampsia, offering a new mouse model for studying the disease.

This paper identifies FSS-dependent enhancers for KLF2 and reveals an essential MEF2-TBP double motif in their regulation, demonstrating a specific mechanism for FSS-induced gene activation.

The paper develops a DNA nanodevice to apply controlled forces to proteins, demonstrating its use in studying mechanosensitive protein interactions and identifying novel tension-dependent binders.

The paper identifies PIEZO1 overexpression in HHT2 AVMs and shows that inhibiting PIEZO1 reduces AVM formation in Alk1-deficient mice.

This study shows LPHN2 is essential for flow-induced Notch activation to suppress inflammation and atherosclerosis in endothelial cells.

This paper identifies Latrophilin-2 as a mediator of flow-induced Smad1/5 activation in endothelial cells through interactions with Endoglin and Shank3, independent of G-proteins.

This study shows that disrupting TGFβ signaling in adult mice makes the aorta susceptible to hypertension-induced dissection, even from short-term blood pressure increases.

This study identifies PRC2 as a driver of atherosclerosis by suppressing Klf2/4, and shows that inhibiting PRC2 with tazemetostat reduces plaque progression and improves stability.

The paper develops a DNA-based molecular clamp to apply tension to proteins and study their interactions and structure under force.

This study identifies latrophilin-2 as an upstream mechanosensor for fluid shear stress in endothelial cells, linking it to vascular development and disease.

This study shows VEGF inhibits arterial specification in capillaries by suppressing Sox17, preventing premature arterialization driven by shear stress.

This study shows that Smad4 loss in endothelial cells leads to AVM formation through flow-induced Klf4 activation and loss of arterial identity.

This study identifies latrophilins as essential for endothelial cell mechanotransduction of fluid shear stress through both G protein-dependent and -independent pathways.