• Publications
  • Influence
Cyclophilin A: a key player for human disease
Recently available data about CyPA in cardiovascular diseases, viral infections, neurodegeneration, cancer, rheumatoid arthritis, sepsis, asthma, periodontitis and aging are discussed.
Cyclophilin A enhances vascular oxidative stress and development of angiotensin II-induced aortic aneurysms
Mechanical studies showed that VSMC-derived intracellular and extracellular CypA are required for ROS generation and matrix metalloproteinase-2 activation, which defines a previously undescribed role for CypA in AAA formation and suggest CypA as a new target for treating cardiovascular disease.
Flow shear stress and atherosclerosis: a matter of site specificity.
The targeted modulation of proteins activated in a site-specific manner holds the promise for a new approach to limit atherosclerosis.
Cyclophilin A is an inflammatory mediator that promotes atherosclerosis in apolipoprotein E–deficient mice
Cyclophilin A promotes atherosclerosis in part by inducing reactive oxygen species and promoting endothelial cell apoptosis and macrophage recruitment into lesions.
Cyclophilin A Mediates Vascular Remodeling by Promoting Inflammation and Vascular Smooth Muscle Cell Proliferation
In response to low flow, CyPA plays a crucial role in VSMC migration and proliferation, as well as inflammatory cell accumulation, thereby regulating flow-mediated vascular remodeling and intima formation.
PKCzeta decreases eNOS protein stability via inhibitory phosphorylation of ERK5.
The results show that PKCζ binds and phosphorylates ERK5, thereby decreasing eNOS protein stability and contributing to early events of atherosclerosis.
Oxidative stress and vascular smooth muscle cell growth: a mechanistic linkage by cyclophilin A.
CyPA plays a crucial role in VSMC proliferation/migration and inflammatory cell recruitment, resulting in cardiovascular diseases in vivo, and is tested by analyzing several genetic interventions that include the CyPA knockout mouse and theCyPA overexpressing transgenic mouse.
Thioredoxin Interacting Protein Promotes Endothelial Cell Inflammation in Response to Disturbed Flow by Increasing Leukocyte Adhesion and Repressing Kruppel-Like Factor 2
The essential role for TXNIP is demonstrated in mediating EC-leukocyte adhesion under d-flow, as well as a novel mechanism by whichTXNIP acts as a transcriptional corepressor to regulate Kruppel-like factor 2-dependent gene expression.