Publications by authors named "Ashley Y Martin"
Article Synopsis
- - Drp1, a protein involved in mitochondrial fission, contributes to the increase in pulmonary artery smooth muscle cells in pulmonary arterial hypertension (PAH), and researchers developed a new inhibitor called Drpitor1a to test its effectiveness.
- - Experiments showed that Drpitor1a successfully inhibited Drp1 activity, reduced cell proliferation and increased apoptosis in PAH cells, while not affecting normal cells or causing toxicity.
- - The findings suggest that Drpitor1a could be a viable treatment for PAH by targeting Drp1, with notable differences in effectiveness observed between male and female subjects.
Background: Mutations are found in 10-20% of idiopathic PAH (IPAH) patients, but none are consistently identified in connective tissue disease-associated PAH (APAH), which accounts for ∼45% of PAH cases. mutations, a cause of clonal hematopoiesis of indeterminant potential (CHIP), predispose to an inflammatory type of PAH. We now examine mutations in another CHIP gene, , in PAH.
View Article and Find Full Text PDFBackground As partial pressure of oxygen (pO) rises with the first breath, the ductus arteriosus (DA) constricts, diverting blood flow to the pulmonary circulation. The DA's O sensor resides within smooth muscle cells. The DA smooth muscle cells' mitochondrial electron transport chain (ETC) produces reactive oxygen species (ROS) in proportion to oxygen tension, causing vasoconstriction by regulating redox-sensitive ion channels and enzymes.
View Article and Find Full Text PDFArticle Synopsis
- SARS-CoV-2, the virus responsible for COVID-19, may harm lung cells by damaging mitochondria, leading to cell death and impaired oxygen regulation in the body.
- The study investigated how SARS-CoV-2 and its proteins affect cell processes like apoptosis (cell death), mitochondrial function, and hypoxic pulmonary vasoconstriction (the body’s way to control blood flow in response to low oxygen).
- Findings showed that SARS-CoV-2 disrupts mitochondrial functions and activates pathways that promote cell death, affecting energy production and overall lung health very shortly after infection.
Macrophage-NLRP3 Activation Promotes Right Ventricle Failure in Pulmonary Arterial Hypertension.
Am J Respir Crit Care Med
September 2022
Pulmonary arterial hypertension (PAH) often results in death from right ventricular failure (RVF). NLRP3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3)-macrophage activation may promote RVF in PAH. Evaluating the contribution of the NLRP3 inflammasome in RV macrophages to PAH RVF.
View Article and Find Full Text PDFBackground: Neutrophils play a role in innate immunity and are critical for clearance of Staphylococcus aureus. Current understanding of neutrophil bactericidal effects is that NADPH oxidase produces reactive oxygen species (ROS), mediating bacterial killing. Neutrophils also contain numerous mitochondria; since these organelles lack oxidative metabolism, their function is unclear.
View Article and Find Full Text PDFAssessment of cardiac function is essential to conduct cardiovascular and pulmonary-vascular preclinical research. Pressure-volume loops (PV loops) generated by recording both pressure and volume during cardiac catheterization are vital when assessing both systolic and diastolic cardiac function. Left and right heart function are closely related, reflected in ventricular interdependence.
View Article and Find Full Text PDFBackground: Pulmonary arterial hypertension (PAH) is a lethal vasculopathy. Hereditary cases are associated with germline mutations in and 16 other genes; however, these mutations occur in <25% of patients with idiopathic PAH and are rare in PAH associated with connective tissue diseases. Preclinical studies suggest epigenetic dysregulation, including altered DNA methylation, promotes PAH.
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