35 research outputs found

    miRNA-140-5p: new avenue for pulmonary arterial hypertension drug development?

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    Pulmonary arterial hypertension (PAH) is a rare but fatal disease. Pathologically, PAH is characterised by sustained vasoconstriction and progressive obliteration of small pulmonary arteries through a process of medial thickening, intimal fibrosis and the formation of angioproliferative lesions. Current treatments target the sustained vasoconstriction via either the prostacyclin, endothelin or nitric oxide pathway but do little to address the underlying progressive proliferative vascular disease. Dysregulated expression of microRNA (miR) has been identified in PAH and we have recently highlighted reduced miR-140-5p in patients with PAH. Replacement of miR-140-5p attenuated disease in animal models with the regulation of Smurf1, a E3 ubiquitin ligase targeting BMPR2 as one identified mechanism. These data highlight Smurf1 inhibition as a treatment for PAH

    Balloon Pulmonary Angioplasty: State of the Art

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    Balloon pulmonary angioplasty (BPA) is a novel technique for the treatment of chronic thromboembolic pulmonary hypertension. While cardiologists need no introduction to the concept of balloon angioplasty, BPA has its own particular challenges. This article aims to provide the reader with an overview of BPA, starting with an introduction to chronic thromboembolic disease (CTED), the standard management of chronic thromboembolic pulmonary hypertension (CTEPH), technical challenges faced when performing BPA and the evidence base supporting its use. The second part of the article will focus on the future of BPA, in particular the areas where research is required to establish an evidence base to justify the role of BPA in CTEPH and CTED treatment

    Protein trafficking through the endosomal system prepares intracellular parasites for a home invasion

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    Toxoplasma (toxoplasmosis) and Plasmodium (malaria) use unique secretory organelles for migration, cell invasion, manipulation of host cell functions, and cell egress. In particular, the apical secretory micronemes and rhoptries of apicomplexan parasites are essential for successful host infection. New findings reveal that the contents of these organelles, which are transported through the endoplasmic reticulum (ER) and Golgi, also require the parasite endosome-like system to access their respective organelles. In this review, we discuss recent findings that demonstrate that these parasites reduced their endosomal system and modified classical regulators of this pathway for the biogenesis of apical organelles
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