Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities.

Acute myocardial infarction (AMI) and the heart failure that often follows, are major causes of death and disability worldwide. As such, new therapies are required to limit myocardial infarct (MI) size, prevent adverse left ventricular (LV) remodeling, and reduce the onset of heart failure following AMI. The inflammatory response to AMI, plays a critical role in determining MI size, and a persistent pro-inflammatory reaction can contribute to adverse post-MI LV remodeling, making inflammation an important therapeutic target for improving outcomes following AMI.

MicroRNA-142 is a multifaceted regulator in organogenesis, homeostasis, and disease.

Over the past decade, microRNA-142 (miR-142) is emerging as a major regulator of cell fate decision in the hematopoietic system. However, miR-142 is expressed in many other tissues, and recent evidence suggests that it may play a more pleiotropic role during embryonic development. In addition, miR-142 has been shown to play important functions in disease.

Quantitative proteome analysis of alveolar type-II cells reveals a connection of integrin receptor subunits beta 2/6 and WNT signaling.

Alveolar type-II cells (ATII cells) are lung progenitor cells responsible for regeneration of alveolar epithelium during homeostatic turnover and in response to injury. Characterization of ATII cells will have a profound impact on our understanding and treatment of lung disease. The identification of novel ATII cell-surface proteins can be used for sorting and enrichment of these cells for further characterization.