A Cardiac Nonproliferation Treaty

摘要

A common basis of human mortality is the heart, arising from morphoge-netic defects of the organ at birth as well as from the chronic ravages of hypertension and coronary artery disease later in life (1). A key pathological mechanism is muscle cell death, mitigated by only a scant capacity for muscle cell renewal. Rescuing cardiac muscle cell number might underlie therapeutic strategies, such as the use of antagonists of muscle cell death, stem cell grafting (now pursued in clinical trials), and activating self-repair by dormant cardiac stem cells in the heart (2).