2020
DOI: 10.1016/j.jprot.2020.103757
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Molecular signatures of atherosclerotic plaques: An up-dated panel of protein related markers

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Cited by 12 publications
(20 citation statements)
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“…ECM degradation, in response to diverse stimulus, leads to degradation or partial modification of matrix molecules, release of soluble peptides, “matrikines”, with pro- or anti-angiogenic activity [ 41 ]. Herein, several matrikines were up-regulated, probably by the action of proteases such as cathepsin D, matrix metallopeptidase 9 (MMP9), or similar molecules that are released in high levels by atherosclerotic plaques (as we and others have previously demonstrated [ 42 ]). Remarkably, many of the up-regulated proteins or peptides in CAC present anti-angiogenic properties, like the proteolytic fragments derived from the C-terminal cleavage of type XV and type XVIII collagens, restin and endostatin, respectively [ 43 ].…”
Section: Discussionmentioning
confidence: 88%
See 1 more Smart Citation
“…ECM degradation, in response to diverse stimulus, leads to degradation or partial modification of matrix molecules, release of soluble peptides, “matrikines”, with pro- or anti-angiogenic activity [ 41 ]. Herein, several matrikines were up-regulated, probably by the action of proteases such as cathepsin D, matrix metallopeptidase 9 (MMP9), or similar molecules that are released in high levels by atherosclerotic plaques (as we and others have previously demonstrated [ 42 ]). Remarkably, many of the up-regulated proteins or peptides in CAC present anti-angiogenic properties, like the proteolytic fragments derived from the C-terminal cleavage of type XV and type XVIII collagens, restin and endostatin, respectively [ 43 ].…”
Section: Discussionmentioning
confidence: 88%
“…We have shown here, for the first time, the effect of atherosclerotic factors over the paracrine role of CAC ex vivo ( Figure 6 ). Our data indicated that the action of proteins secreted in high levels by atherosclerotic plaques such as proteases like Cathepsin D or MMP9 [ 42 ], promotes the release by CAC of several proteins or peptide fragments mainly from the ECM and basement membrane (fibulins, restin, endostatin, thrombospondins, latent TGFβ binding proteins, among others). Many of these proteins have been described as strong anti-angiogenic factors, and they might be responsible for promoting an angiogenic switch by impairing ECFC tubule formation ex vivo, as we saw in our functional assays.…”
Section: Discussionmentioning
confidence: 99%
“…Currently, there are numerous novel imaging techniques that can detect potentially unstable plaques: magnetic resonance imaging, high-resolution computed tomography, positron emission tomography and contrast-enhanced ultrasound (7)(8)(9)(10)(11). Processes indicating plaque activity (molecular imaging) such as: glucose absorption, protein degradation, exposure of adhesive molecules or content of markers for apoptosis are tested for use in the diagnosis of plaques at risk of destabilization (12)(13)(14)(15).…”
Section: Introductionmentioning
confidence: 99%
“…Plaque instability, in which the activation of proteases for extracellular matrices and the loss of VSMCs are involved, increases the risk of cardiovascular events [ 4 ]. Because these pathological changes in the vascular wall are mostly asymptomatic, the detection of atherosclerotic lesions by serological biomarkers before critical clinical features emerge has been extensively investigated [ 5 , 6 , 7 , 8 , 9 ].…”
Section: Introductionmentioning
confidence: 99%