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Maja Bundalo on Muck Rack

Maja Bundalo

As seen in: BioRxiv
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Articles

Blocking Interleukin-1β transiently limits left ventricular dilation and reduces cardiac lymphangiogenesis during pressure-overload in mice

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By Coraline Héron, Theo Lemarcis, Oceane Laguerre, Maja Bundalo
| BioRxiv
Abstract Blocking pro-inflammatory pathways, e.g. the inflammasome or interleukin (IL)-1β, is a promising therapeutic approach in heart failure (HF). We hypothesized that IL-1β may regulate cardiac lymphangiogenesis in response to chronic pressure-overload, and hence could impact the resolution of myocardial edema and inflammation and the development of cardiac fibrosis and HF.
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Redirecting full-length FLT1 expression towards its soluble isoform promotes postischemic angiogenesis

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By Maja Bundalo, Sandra Vorlova, Jessica Ulrich, Ruggero Barbieri
| BioRxiv
Abstract Vascular endothelial growth factors and their tyrosine kinase receptors are key mediators of vasculogenesis and angiogenesis with FLT1 (VEGFR1) serving as a decoy receptor. A truncated mRNA transcript encoding soluble (s) FLT1 can be generated by premature cleavage and polyadenylation (APA).
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Blocking Interleukin-1beta transiently limits left ventricular dilation and reduces cardiac lymphangiogenesis in a mouse pressure-overload model

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By Coraline Héron, Theo Lemarcis, Oceane Laguerre, Maja Bundalo
| BioRxiv
Abstract Blocking inflammatory pathways, e.g. the inflammasome or interleukin (IL)-1beta, is a promising therapeutic approach in heart failure (HF). We hypothesized that IL-1β may stimulate cardiac lymphangiogenesis in response to left ventricular (LV) dilation following pressure-overload. Consequently, blocking IL-1βbeta may reduce lymphangiogenesis, delaying resolution of myocardial edema and inflammation, aggravating cardiac fibrosis, and accelerating HF development.
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