fig3

Microvesicles and exosomes in pulmonary hypertension

Figure 3. This figure depicts the possible mechanism of injury resulting in dysregulation of a number of vascular and inflammatory cells. Injury (inflammatory, oxidant, drug toxicity, increased pulmonary flow) activates Plt, Leuk and EC to produce increased amounts of EVs. EVs from platelets and leukocytes induce EC dysfunction. Endothelial EVs contain inflammatory and proliferative factors, and miRNAs are incorporated in SMCs, leading to hypertrophy, proliferation and phenotype change. These SMCs produce EVs containing TGFβ, miRNAs and other factors that are incorporated into ECs, leading to EndMT. EC: endothelial cell; EVs: extracellular vesicles; SMCs: smooth muscle cells; EndMT: endothelial mesenchymal transition; Plt: platelets; Leuk: leukocytes; TGFβ: transforming growth factor β

Vessel Plus
ISSN 2574-1209 (Online)
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