Journal
KIDNEY INTERNATIONAL
Volume 93, Issue 2, Pages 298-301Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.kint.2017.08.036
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Funding
- Plan Estatal de I+D+I, Instituto de Salud Carlos III (ISCIII) Fondo Europeo de Desarrollo Regional (FEDER) [PI14/01452]
- Plan de Ciencia, Tecnologia e Innovacion del Principado de Asturias [GRUPIN14-028]
- Fundacion para el Fomento en Asturias de la Investigacion Cientifica Aplicada a la Tecnologia (FICYT)
- Red de Investigacion Renal-REDinREN from ISCIII [RD06/0016/1013, RD12/0021/1023]
- Sociedad Asturiana Fomento Investigaciones Metabolicas (SAFIM)
- Agencia [PICT 2013-0305]
- Sectyp (U.N.CUYO)
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Prevention of medial calcification in patients with chronic kidney disease requires the maintenance of vascular smooth muscle cell fitness. To preserve viability under chronic kidney disease-induced stress, vascular smooth muscle cells increase exosome formation and release, but the result is aggravated pathological calcification. Now Chen et al. report that microvesicles from calcifying vascular smooth muscle cells may propagate procalcifying signals to normal vascular smooth muscle cells. To help design effective strategies to impair procalcifying cell-to-cell communication, this commentary updates the current understanding of the main regulators of microvesicle/exosome biogenesis and secretion.
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