Macrophages regulate salt-dependent volume and blood pressure by a vascular endothelial growth factor-C–dependent buffering mechanism

By A. Machnik, W. Neuhofer, J. Jantsch, Anke Dahlmann, T. Tammela, K. Machura, Joon-Keun Park, F. Beck, D. Müller, W. Derer and 12 more. Nature Medicine, 2009

929 citations recorded by the source corpus.

Subfields: Endocrine and Autonomic Systems, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/02343e88c40e97ccd1a6296c57b4aac5a7ab9ded

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Oncology

1. H. Wiig
2. M. Swartz
3. K. Alitalo
4. T. Tammela
5. Rakesh K. Jain
6. M. Shibuya

In Physiology

1. T. Tammela
2. K. Alitalo

Citations in the corpus

• Lymphangiogenesis: Molecular mechanisms and future promise. (2010, background): “Recent exciting work by Machnik et al. suggests that the lymphatic vessels proliferate in response to a high-salt diet, possibly via upregulation of VEGF-C in monocytic cells infiltrating the interstitium of the skin (Machnik et al., 2009).”
• The lymphatic vasculature in disease (2011, background): “Recent results have shown that hypertension induced by salt overload leads to inflammatory cell recruitment and increased lymphangiogenic growth factor production in the ski”
• Interstitial fluid and lymph formation and transport: physiological regulation and roles in inflammation and cancer. (2012, background): “Later experiments have suggested that the response to high salt is orchestrated by activation of tonicity-responsive enhancer binding protein (TonEBP) in infiltrating macrophages, that in addition to change in GAG charge density and amount results in VEGF-C secretion and hyperplasia of the lymph cap”