Table 4.

Key knowledge gaps in the assessment of angiogenesis in the RV

What are the molecular regulators of RV angiogenesis (proangiogenic and angiostatic)?

Is angiogenesis necessary and sufficient to induce RV cardiomyocyte hypertrophy?

Does decreased angiogenesis contribute to maladaptive remodeling in the RV?

How should we define adaptive remodeling in the RV?

How should we define maladaptive remodeling in the RV?

What methodological approach should we use to measure RV function vs failure?

What is the most accurate methodological approach to quantifying RV vascularization?

Are we introducing unintentional sampling bias into our traditional approaches to capillary density?

Does the use of different RV endothelial cell markers (CD31, von Willebrand factor, or lectin) between researchers introduce bias to our quantification of capillaries?

How do interventions targeting the pulmonary vasculature affect the vasculature of the RV? How do interventions targeting the RV vasculature affect the pulmonary vasculature? Can these compartments be targeted separately?

How can we maximize results from the study of RV angiogenesis in vitro? What can we learn from studies of RV cardiomyocyte-endothelial cell interactions on a chip or from iPSC-cardiomyocytes from PH patients?

How can we maximize the collection of human RV tissue from well phenotyped patients and controls?

How can we best monitor RV vascular function in clinical studies?

RV, right ventricle.