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NEW RESEARCH

VEGF-B: A more balanced approach to cardiac angiogenesis?

A new study undertaken at UiB does answer one set of questions, however, raises many more with regards to the potential use of specific VEGF isoforms in order to promote re-vascularisation in heart failure.

VEGF-B overexpressing heart is sensitized to develop heart failure in DOCA-salt hypertensive rats
VEGF-B overexpressing heart is sensitized to develop heart failure in DOCA-salt hypertensive rats (A) BP recordings of free moving rats using radiotelemetry (DSI). (B) Electrolyte measurements in heart and plasma. (C) Cardiac structure and function using Echocardiography. (D) Different functions of vascular endothelial growth factor receptors. VEGFB binding to VEGFR1 promotes tissue remodeling and cell survival and indirect promote angiogenesis via activation of VEGFA –VEGFR2 signaling pathway.
Photo:
Anne-Maj Samuelsson

What is angiogenesis within the realm of heart disease? Angiogenesis is the process whereby new blood vessels are formed, improving ischemic tissue function and thereby considering as potential therapy for patients with heart failure. Preclinical studies have pointed towards vascular growth factor A (VEGF-A). However, few significant studies have been undertaken and many obstacles remain (enhanced vascular permeability and inflammation). In collaboration with Prof. Alitalo (University of Helsinki), Dr Samuelsson of Prof. Wiig’s group headed a preclinical study of VEGF-B, being a growth factor less familiar than its counterpart A. Recent findings were presented at the Physiology Society meeting at Reykjavik, Iceland in August 2019.

VEGF-B has been shown to activate genes involved in the regulation of myocardial contractility and metabolism, as well as protect against ischemia through re- vascularisation and hypertrophy. However, the timing and duration of the VEGF-B appears essential with longer VEGF-B expression leading to adverse heart muscle remodeling, excitation and, paradoxically, heart failure. The proteomic analysis indicates an early pathological sacromere along with actin filament dysfunction, which might lead to compensatory hypertrophy and vascular remodeling. VEGF-B hence offers a new perspective on heart failure research with the focal point being tissue remodeling with a view to improve heart function and offer further clinical benefits.