Emerging multimodality imaging techniques for the pulmonary circulation.
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2024-10
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Pulmonary hypertension (PH) remains a challenging condition to diagnose, classify and treat. Current approaches to the assessment of PH include echocardiography, ventilation/perfusion scintigraphy, cross-sectional imaging using computed tomography and magnetic resonance imaging, and right heart catheterisation. However, these approaches only provide an indirect readout of the primary pathology of the disease: abnormal vascular remodelling in the pulmonary circulation. With the advent of newer imaging techniques, there is a shift toward increased utilisation of noninvasive high-resolution modalities that offer a more comprehensive cardiopulmonary assessment and improved visualisation of the different components of the pulmonary circulation. In this review, we explore advances in imaging of the pulmonary vasculature and their potential clinical translation. These include advances in diagnosis and assessing treatment response, as well as strategies that allow reduced radiation exposure and implementation of artificial intelligence technology. These emerging modalities hold the promise of developing a deeper understanding of pulmonary vascular disease and the impact of comorbidities. They also have the potential to improve patient outcomes by reducing time to diagnosis, refining classification, monitoring treatment response and improving our understanding of disease mechanisms.
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Rajagopal, Sudarshan, Harm J Bogaard, Mohammed SM Elbaz, Benjamin H Freed, Martine Remy-Jardin, Edwin JR van Beek, Deepa Gopalan, David G Kiely, et al. (2024). Emerging multimodality imaging techniques for the pulmonary circulation. The European respiratory journal, 64(4). p. 2401128. 10.1183/13993003.01128-2024 Retrieved from https://hdl.handle.net/10161/34044.
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Sudarshan Rajagopal
I am a physician-scientist with a research focus on G protein-coupled receptor signaling in inflammation and vascular disease and a clinical focus on pulmonary vascular disease, as I serve as Co-Director of the Duke Pulmonary Vascular Disease Center. My research spans the spectrum from clinical research in pulmonary vascular disease, to translational research in cardiovascular disease, to the basic science of receptor signaling.
Our basic science resesarch focuses on understanding and untapping the signaling potential of G protein-coupled receptors (GPCRs) to regulate inflammation in vascular disease. GPCRs are the most common transmembrane receptors in the human genome (over 800 members) and are some of the most successful targets for drug therapies. While it has been known for some time that these receptors signal through multiple downstream effectors (such as heterotrimeric G proteins and multifunctional beta arrestin adapter proteins), over the past decade it has been better appreciated that these receptors are capable of signaling with different efficacies to these effectors, a phenomenon referred to as “biased agonism”. Ligands can be biased, by activating different pathways from one another, and receptors can be biased, by signaling to a limited number of pathways that are normally available to them. Moreover, this phenomenon also appears to be common to other transmembrane and nuclear receptors. While a growing number of biased agonists acting at multiple receptors have been identified, there is still little known regarding the mechanisms underlying biased signaling and its physiologic impact.
Much of our research focuses on the chemokine system, which consists of approximately twenty receptors and fifty ligands that display considerable promiscuity with each other in the regulation of immune cell function in inflammatory diseases. Research from our group and others have shown that many of these ligands act as biased agonists when signaling through the same receptor. We use models of inflammation such as contact hypersensitivity and pulmonary arterial hypertension (PAH). PAH is a disease of the pulmonary arterioles that results in right heart failure and most of its treatments target signaling by GPCRs. We use multiple approaches to probe these signaling mechanisms, including in-house pharmacological assays, advanced phosphoproteomics and single cell RNA sequencing.
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