• Publications
  • Influence
Endothelial dysfunction in cardiovascular diseases: the role of oxidant stress.
TLDR
Accumulating evidence suggests that oxidant stress alters many functions of the endothelium, including modulation of vasomotor tone, and as the role of these various enzyme sources of ROS become clear, it will perhaps be possible to use more specific therapies to prevent their production and ultimately correct endothelial dysfunction. Expand
The vascular NAD(P)H oxidases as therapeutic targets in cardiovascular diseases.
TLDR
Investigating the mechanisms of activation of the endothelial and vascular smooth muscle NAD(P)H oxidases in mice that are deficient in p47(phox) and gp91( phox) shows that ROS produced by these oxidases contribute to cardiovascular diseases including atherosclerosis and hypertension. Expand
Hydrogen peroxide regulation of endothelial function: origins, mechanisms, and consequences.
  • H. Cai
  • Biology, Medicine
  • Cardiovascular research
  • 1 October 2005
Increased production of reactive oxygen species (ROS) has been implicated in the pathogenesis of cardiovascular diseases. Enzymatic systems such as the mitochondrial respiratory chain, vascularExpand
Sex difference and smoking predisposition in patients with COVID-19
  • H. Cai
  • Medicine
  • The Lancet Respiratory Medicine
  • 11 March 2020
TLDR
The current literature does not support smoking as a predisposing factor in men or any subgroup for infection with SARS-CoV-2, but there might be a sex predisposition to COVID-19, with men more prone to being affected. Expand
Endothelial dihydrofolate reductase: critical for nitric oxide bioavailability and role in angiotensin II uncoupling of endothelial nitric oxide synthase.
  • K. Chalupský, H. Cai
  • Chemistry, Medicine
  • Proceedings of the National Academy of Sciences…
  • 21 June 2005
TLDR
Findings that specific inhibition of endothelial DHFR by RNA interference markedly reduced endothelial H4B and nitric oxide (NO.) bioavailability are presented and represent evidence that DHFR is critical for H 4B and NO. Expand
Akt-dependent phosphorylation of serine 1179 and mitogen-activated protein kinase kinase/extracellular signal-regulated kinase 1/2 cooperatively mediate activation of the endothelial nitric-oxide
TLDR
H( 2)O(2) causes endothelial NO* release mediated by cooperative effects between PI 3-kinase/Akt-dependent eNOS serine 1179 phosphorylation and activation of MEK/ERK1/2, which may represent an acute cellular adaptation to an increase in oxidant stress. Expand
Shear Stress Regulates Endothelial Nitric Oxide Synthase Expression Through c-Src by Divergent Signaling Pathways
In this study, we defined the signaling cascade responsible for increased eNOS mRNA expression in response to laminar shear stress. This pathway depends on the tyrosine kinase c-Src because shearExpand
Netrin-1 induces angiogenesis via a DCC-dependent ERK1/2-eNOS feed-forward mechanism.
  • Andrew Nguyen, H. Cai
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences…
  • 25 April 2006
TLDR
It is reported that netrin-1 induction of angiogenesis is mediated by an increase in endothelial nitric oxide (NO*) production, which occurs via a DCC-dependent, ERK1/2-eNOS feed-forward mechanism. Expand
Transcriptional and posttranscriptional regulation of endothelial nitric oxide synthase expression by hydrogen peroxide.
TLDR
H( 2)O(2) increases eNOS expression through transcriptional and post-transcriptional mechanisms and is likely to be involved in regulation of eN OS expression in response to other physiological and/or pathophysiological stimuli. Expand
Endothelium-specific overexpression of class III deacetylase SIRT1 decreases atherosclerosis in apolipoprotein E-deficient mice.
TLDR
It is suggested that endothelium-specific SIRT1 overexpression likely suppresses atherogenesis via improving endothelial cell survival and function. Expand
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