Research Focus: Part 2

Last week’s blog post took a look at two areas that Stephen M. Black is currently researching: Perinatal regulation of endothelial NOS, and Perinatal regulation of TGF-beta1 during vascular remodeling. However, there are many more research projects on which Stephen M. Black and his integrated cardiovascular laboratory are focusing. Most of his research, which extramurally funded by outside parties, is intended to help the medical community gain a better understanding of how reactive nitrogen species (RNS) generations alters function both in a living organism (in vitro) and in a test tube environment (in vivo). Ongoing research projects that have not previously been discussed are:


Role of altered carnitine metabolism in perinatal endothelial dysfunction

Based on Stephen M. Black’s recent study involving a lamb model of congenital heart disease and increased pulmonary blood flow, the development of endothelial dysfunction has been shown to be associated with derangements (disruptions) in nitric oxide (NO) signaling. Since the mechanisms by which endothelial dysfunction occurs have not been adequately resolved, this study aims to do two things: reveal the mechanisms that underlie disruption of carnitine metabolism in the previously mentioned lamb model, and utilize L-carnitine (a compound used for decades to treat inborn metabolism errors) as a therapeutic agent for the endothelial dysfunction associated with congenital heart disease. The study’s results should provide the medical community with a better understanding of the role mitochondrial dysfunction plays in congenital heart disease and determine if L-carnitine is an effective treatment strategy.

ROS in pulmonary hypertension: role of ADMA

In previous studies involving a lamb model, Stephen M. Black has shown that increased reactive oxygen species (ROS) generation in the pulmonary vessels influences the development of pulmonary hypertension. New preliminary data shows that increased ROS generation also correlates with an elevation in asymmetric dimethyl arginine (ADMA) levels and a decrease in tetrahydrobiopterin (BH4) levels. This study should elucidate the medical commuity’s understanding of the role ADMA plays in the mitochondrial dysfunction process, and how diminied NO-signaling and endothelial dysfunction trigger pulmonary hypertension secondary to increased pulmonary blood flow. This study could also suggest new signaling pathways that improve treatment of infants and children with pulmonary hypertension.

These are just two of the many active research projects on which Stephen M. Black is focused. Learn more about his research by reading some of the questions he has answered on his Quora.


  1. […] to expand our knowledge of conditions such as congenital heart disease and pulmonary hypertension. Last week’s blog post focused on two such research projects: Role of altered carnitine metabolism in perinatal […]

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