JCI table of contents: Nov. 1, 2007

TITLE: Cardiomyocyte GATA4 functions as a stress-responsive regulator of angiogenesis in the murine heart

AUTHOR CONTACT:
Jeffery D. Molkentin
Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Phone: (513) 636-3557; Fax (513)-636-5958; E-mail: .

View the PDF of this article at: https://www.the-jci.org/article.php?id=32573

RELATED MANUSCRIPT

TITLE: Myocardial hypertrophy in the absence of external stimuli is induced by angiogenesis in mice

AUTHOR CONTACT:
Michael Simons
Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, USA.
Phone: (603) 650-3540; Fax: (603) 650-5171; E-mail: .

View the PDF of this article at: https://www.the-jci.org/article.php?id=32024

ACCOMPANYING COMMENTARY

TITLE: Cardiac growth and angiogenesis coordinated by intertissue interactions

AUTHOR CONTACT:
Kenneth Walsh
Boston University School of Medicine, Boston Massachusetts, USA.
Phone: (617) 414-2390; Fax: (617) 414-2391; Email: .

View the PDF of this article at: https://www.the-jci.org/article.php?id=34126

NEPHROLOGY: I(r)oning out the mechanisms of kidney functions

One of the functions of the kidneys is to maintain an optimal concentration in the body of charged molecules known as ions. Maintaining these at the correct concentration is important for the function of all cells in the body, as well as for maintaining whole body function. For example, the concentration of sodium ions (Na+), which are derived from salt we consume, affects blood pressure -- increased Na+ concentrations increase blood pressure. In the November issue of the Journal of Clinical Investigation, two studies have determined the molecular mechanisms by which the function of two ion transporters primarily expressed in the kidneys are regulated. The commonalities behind these mechanisms and their clinical implications are discussed in the accompanying commentary by Juerg Biber and colleagues at the University of Zurich, Switzerland.

In the first study, David Ellison and colleagues from Oregon Health & Science University, Portland, show that in Xenopus oocytes and human kidney cells, thiazide-sensitive Na-Cl cotransporter (NCC) -- inappropriate activation of which has been recently linked to familial hyperkalemic hypertension (an inherited condition characterized by high blood pressure) -- is regulated by a number of proteins known as WNKs. Interactions between WNK3 and WNK4 were found to fine-tune the function of NCC.