News From The Journal Of Clinical Investigation: Jan. 24, 2012

Main Category: Urology / Nephrology
Also Included In: Vascular;  Men's health
Article Date: 25 Jan 2012 - 1:00 PST

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NEPHROLOGY: Understanding acute kidney injury to identify potential therapeutics

Acute kidney injury (AKI) is a life-threatening condition that frequently complicates the care of hospitalized patients. There are no specific therapies to treat AKI other than kidney replacement therapies such as dialysis. Better understanding of the molecular mechanisms underlying AKI is needed if effective new therapies are to be developed. In this context, a team of researchers led by Holger Eltzschig, at the University of Colorado Denver, Aurora, has now dissected the role of the molecule adenosine in mice exposed to AKI caused by transient obstruction to the blood flow to the kidney, the most common cause of AKI in patients. In doing so, Eltzschig and colleagues identified activators of the A2B adenosine receptor and inhibitors of the protein ENT1, which is involved in transporting adenosine into and out of cells in the kidney, as potential therapeutics for AKI, although they caution that mice are not humans and that much work is needed to see if their results in mice hold up in humans.

In an accompanying commentary, Joel Weinberg (at the University of Michigan, Ann Arbor) and Manjeri A. Venkatachalam (at University of Texas Health Science Center at San Antonio, San Antonio) discuss the complexities of the work performed by Eltzschig and colleagues and the relevance of the data to the human condition.

TITLE: Equilibrative nucleoside transporter 1 (ENT1) regulates postischemic blood flow during acute kidney injury in mice

View this article at: http://www.jci.org/articles/view/60214?key=08d041baa97863b6dc1d

ACCOMPANYING COMMENTARY TITLE: Preserving postischemic reperfusion in the kidney: a role for extracellular adenosine

View this article at: http://www.jci.org/articles/view/60957?key=80692b200000946d601d

VASCULAR DISEASE: Triple A rating for gene regulatory molecule miR-29b

Abdominal aortic aneurysms (AAAs) are an abnormal widening or ballooning of the lower part of the body's main artery (the aorta) due to weakness in its wall. They are a common clinical condition, occurring primarily in men over the age of 65 years, that can cause death due to dissection or rupture of the aorta at the site of the aneurysm. Treatment depends on the size of the aneurysm at diagnosis - patients with small aneurysms are treated using a watch-and-wait approach while those with large aneurysms require surgery. A team of researchers led by Philip Tsao, at Stanford University School of Medicine, Stanford, has now generated data in two mouse models of AAA that suggest that manipulating levels of the gene regulatory molecule miR-29b and the levels of the genes it regulates could help limit AAA progression and protect from rupture.

In an accompanying commentary, Dianna Milewicz, at The University of Texas Health Science Center at Houston, Houston, discusses the data generated by Tsao and colleagues in light of other recent work investigating the role of miR-29 in aortic aneurysm formation.

TITLE: Inhibition of microRNA-29b reduces murine abdominal aortic aneurysm development

View this article at: http://www.jci.org/articles/view/61598?key=3b5048699eed1374fb09

ACCOMPANYING COMMENTARY TITLE: MicroRNAs, fibrotic remodeling, and aortic aneurysms

View this article at: http://www.jci.org/articles/view/62204?key=cfe9473356166fc23dff

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