Karina Yaniv’s Lab

Decoding Vascular & Lymphatic Networks

Research

Our research focuses on the molecular and cellular mechanisms governing the development and function of blood and lymphatic vessels. Using advanced genetic, molecular, and imaging approaches, primarily in zebrafish models, we investigate how vascular systems form, remodel, and function during development, and how these processes go awry in disease.

The lab is particularly interested in angiogenesis and lymphangiogenesis in the context of cardiovascular disease, inflammation tissue regeneration and rare diseases. By uncovering fundamental biological principles of vascular biology, our work aims to bridge basic science with translational relevance.

We are committed to scientific excellence, interdisciplinary collaboration, and training the next generation of researchers in a supportive and innovative research environment.

Research page

From Vascular Disorders to Treatment Discovery

Organ-Specific Vascular Functions in Health, Disease, and Repair

Building and Remodeling Specialized Vascular Networks

News

January 24, 2026

A Major Achievement: Gal Perlmoter’s Thesis Defense

October 8, 2025

Fish That Sparked a Breakthrough at Sheba Medical Center

All News

Selected Publications

A high-throughput zebrafish screen identifies novel candidate treatments for kaposiform lymphangiomatosis (KLA)

Bassi I., Jabali A., Levin L., Lambiase G., Moshe N., Farag N., Tevet Y., Perlmoter G., Egozi S., Leichner G. S., Geva P., Barzilai A., Avivi C., Long J., Otterstrom J. J., Paran Y., Barr H., Yaniv K. & Greenberger S. (2025) Journal of Experimental Medicine. 222, 11, e20240513.

Submitted version

Kaposiform lymphangiomatosis (KLA) is a rare and aggressive disease caused by a somatic activating NRAS mutation (p.Q61R) in lymphatic endothelial cells (LECs). The development of new therapeutic avenues is hampered by the lack of animal models faithfully replicating the clinical manifestations of KLA. Here, we established a novel zebrafish model of KLA by conditionally expressing the human NRAS mutation in venous and lymphatic ECs. Mutant embryos recapitulate key clinical features of KLA, including dilated lymphatics and pericardial edema, which are reversed by trametinib, a MEK inhibitor used in KLA treatment. Leveraging this model in combination with an AI-based high-throughput drug screening platform, we identify cabozantinib, a tyrosine kinase inhibitor, and GSK690693, a competitive pan-Akt kinase inhibitor, as promising candidates for treating KLA. Notably, both drugs normalized sprouting and migration of cultured LECs from a KLA patient. Overall, our novel zebrafish model provides a powerful platform to dissect KLA pathogenesis and identify new therapeutic avenues.

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