Loss of ADAM15 Exacerbates Transition to Decompensated Myocardial Hypertrophy and Dilation Through Activation of the Calcineurin Pathway.

Background: Myocardial hypertrophy and dilation are key features of cardiomyopathies and involve several cellular and molecular events. ADAMs (a disintegrin and metalloproteinases) are membrane-bound proteinases with diverse functions whose role in heart disease remains underexplored. ADAM15 is expressed in the heart and is downregulated in the failing human heart.

ADAM15 is required for optimal collagen cross-linking and scar formation following myocardial infarction.

Collagen cross-linking is an important step in optimal scar formation. Myocardial infarction (MI) results in loss of cardiomyocytes that are replaced with a scar (infarct) tissue. Disintegrin and metalloproteinases (ADAMs) are membrane-bound proteases that can interact with molecules intra- and extra-cellularly to mediate various cellular functions.

Sex- and age-specific regulation of ACE2: Insights into severe COVID-19 susceptibility.

Aged males disproportionately succumb to increased COVID-19 severity, hospitalization, and mortality compared to females. Angiotensin-converting enzyme 2 (ACE2) and transmembrane protease, serine 2 (TMPRSS2) facilitate SARS-CoV-2 viral entry and may have sexually dimorphic regulation. As viral load dictates disease severity, we investigated the expression, protein levels, and activity of ACE2 and TMPRSS2.

Diverse origins and activation of fibroblasts in cardiac fibrosis.

Cardiac fibroblasts (cFBs) have emerged as a heterogenous cell population. Fibroblasts are considered the main cell source for synthesis of the extracellular matrix (ECM) and as such a dysregulation in cFB function, activity, or viability can lead to disrupted ECM structure or fibrosis. Fibrosis can be initiated in response to different injuries and stimuli, and can be reparative (beneficial) or reactive (damaging).