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Blocking p38 MAPK

By Paul Schumacker, PhD, editor, American Journal of Respiratory Cell and Molecular Biology
Follow Dr. Schumacker on Twitter @AJRCMB

p38 MAPK Inhibition Improves Heart Function in Pressure-Loaded Right Ventricular Hypertrophy

A class of mitogen-activated protein kinases known as p38 MAPK play a role in ischemic heart and other diseases. In their November American Journal of Respiratory Cell and Molecular Biology paper, Baktybek Kojonazarov and colleagues hypothesized that p38 MAPK might also play a role in the pathobiology of right ventricular (RV) hypertrophy and failure. In both mice and humans, the authors write, p38 MAPK is “markedly increased” in those with hypertrophied or failed right ventricles, and RV function is the most important determinant of survival in patients with pulmonary arterial hypertension. After inhibiting p38 MAPK in mice, the researchers found that RV function was improved and RV fibrosis was inhibited “via attenuation of MRTF-A [myocardin-related transcription factor] translocation from the cytosol to the nucleus and partly via inhibition of SMAD3 [decapentaplegic homolog 3] activation.”

November Highlights

Translational Review: Cardiomyocytes of the Heart and Pulmonary Veins: Novel Contributors to Asthma?

Unbiased Quantitation of Alveolar Type II to Alveolar Type I Cell Transdifferentiation during Repair after Lung Injury in Mice

Human CD8+ T Cells Damage Noninfected Epithelial Cells during Influenza Virus Infection In Vitro

Critical Role of IRAK-M in Regulating Antigen-Induced Airway Inflammation

Intermittent Hypoxia and Hypercapnia Accelerate Atherosclerosis, Partially via Trimethylamine-Oxide

Restoration of Megalin-Mediated Clearance of Alveolar Protein as a Novel Therapeutic Approach for Acute Lung Injury


November 2017