Abstract
This editorial refers to ‘Exosomes induce and reverse monocrotaline-induced pulmonary hypertension in mice’ by J.M. Aliotta et al ., pp. 319–330. Exosomes form part of the extracellular vesicle (EV) pool, consisting of different cell-derived structures generated from cytoplasmic and membrane components of their source cells. Exosomes are small membrane vesicles (30–100 nm) and can be released from multi-vesicular bodies spontaneously or in response to external signals, such as mechanic and chemical stimuli. Exosomes, like other EV, can act as inter-cellular messengers delivering different RNA species (e.g. miRNA) and proteins to remote organs and cells.1 Accordingly, exosomes can influence multiple biological processes such as immune responses2,3 or tumour growth4 and consequently have gained much attention as therapeutic targets. However, one must not be blind sighted by their potential beneficial effects. In this issue of Cardiovascular Research , Aliotta and co-workers5 extended their previous work on pulmonary hypertension (PAH) in mice by now pinpointing exosomes as the culprit EV fraction when inducing PAH by EV injection derived from monocrotaline (MCT)-treated mice.6 Infusion of the exosome …
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