Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Heart disease is the number one cause of death in the United States, and this month's installment of our 10th anniversary focus series homes in on cardiovascular disease. On page 467, Eric Olson casts the past decade's progress in cardiovascular research in historical perspective. Special news features, a historical News and Views and historical Research Notes round out our special content. Cover image depicts the human heart, courtesy of Getty images.
Ultraviolet radiation thwarts graft-versus-host disease in mice after hematopoietic stem cell transplantation. The treatment kills host Langerhans cells in the skin, which contribute to this deadly disease (pages 510–517).
Increasing sodium absorption by overexpressing the epithelial sodium channel in mouse airways results in mucus accumulation and inflammation, changes that occur in the lungs of individuals with cystic fibrosis. The development of lung disease in these mice should provide insights into a disease that has long been lacking an animal model (pages 487–493).
Fat cells secrete the hormone adiponectin, which regulates glucose metabolism through actions on peripheral tissues. It is now apparent that adiponectin also acts on the brain to reduce body weight and improve glucose metabolism (pages 524–529).
Defects in a Golgi protein, COG7, underlie a disorder that kills children in the first year of life. The disorder is the first to be defined in a class that will likely expand with future studies (pages 518–523).
Signaling through costimulatory receptors classically occurs in cells of the immune system. Now the distinction between immune cells and osteoclasts, bone resorbing cells, begins to blur. Osteoclasts need costimulatory signals too.
Hypothermia resulting from impaired glucose metabolism may be one of the factors that contribute to hyperphosphorylation of the protein tau and subsequent neuronal dysfunction.
In 1995, Mark Keating and colleagues identified two genes responsible for congenital long QT syndrome, a cause of sudden cardiac death. Perturbations in the ion channels that orchestrate the beating heart were central to the disorder. This revelation provided a molecular model for the study of ventricular arrhythmias and enabled further dissection of the genetic defects underlying subtleties in the cardiac phenotype. Soon, these discoveries will be further translated to clinical medicine, with the expected release of one of the first comprehensive clinical genetic tests in cardiology.