04/03/2014 - 14:40

Combating the tissue degrading enzymes that cause lasting damage following a heart attack is tricky. Each patient responds to a heart attack differently and damage can vary from one part of the heart muscle to another, but existing treatments can’t be fine-tuned to deal with this variation.


04/02/2014 - 21:48

The mammalian heart has generally been considered to lack the ability to repair itself after injury, but a 2011 study in newborn mice challenged this view, providing evidence for complete regeneration after resection of 10% of the apex, the lowest part of the heart. In a study published by Cell Press in Stem Cell Reports on April 3, 2014, researchers attempted to replicate these recent findings but failed to uncover any evidence of complete heart regeneration in newborn mice that underwent apex resection.


03/17/2014 - 08:51

A gene termed TM6SF2 has been identified as important in affecting cholesterol levels and myocardial infarction in a new study published as an advanced online publication in Nature Genetics. The study, from scientists in Norway and in the University of Michigan offers a promising new drug target in cardiovascular disease.


02/28/2014 - 10:55

Chronic kidney disease affects 26 million Americans, but its sufferers are more likely to die of heart disease than kidney problems. However, it hasn’t been clear just how kidney disease causes heart disease or what could be done to stop it.


02/28/2014 - 10:18

Early but not advanced forms of atherosclerotic plaques in the vessel wall disappear when the levels of ‘bad’ cholesterol are lowered, according to a study in mice from Karolinska Institutet, Sweden. The findings, published in  PLoS Genetics , indicate that preventative cholesterol-lowering treatment could prevent more advanced, clinically relevant plaque to develop.


02/27/2014 - 11:00

You might think building muscle is a good thing, but that's often not so in the case of blood vessels in adults. In fact, excess smooth muscle is a root problem in many vascular diseases, as it causes arteries to constrict and blood pressure to rise. Now, an in-depth analysis of arterioles in mice with pulmonary hypertension explains how those misplaced smooth muscle cells develop.