Searching for Atherosclerosis Biomarkers by Proteomics: A Focus on Lesion Pathogenesis and Vulnerability

Nieddu, Gabriele; Formato, Marilena; Lepedda, Antonio Junior

doi:10.3390/ijms242015175

Cited by 3 publications

(3 citation statements)

References 184 publications

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“…The study conducted by Loftus et al [50] about the expression of MMP-9 within this tissue demonstrated a significant increase in MMP-9 localized in the most unstable carotid plaques and the plaques of more symptomatic patients. Interestingly, MMP-9 has been considered an excellent candidate for future pharmacotherapy intended to stabilize carotid plaques and prevent stroke [86].…”

Section: Plaque Ulcerationmentioning

confidence: 99%

Molecular Pathways of Vulnerability Carotid Plaques at Risk for Ischemic Stroke: A Narrative Review

Miceli,

Basso,

Pintus

et al. 2024

Preprint

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The concept of vulnerable carotid plaques is pivotal in understanding the pathophysiology of is-chemic stroke secondary to large-artery atherosclerosis. At the macroscopic evaluation, vulnera-ble plaques are characterized by one or more of the following features: microcalcification, neo-vascularization, lipid-rich necrotic core (LRNC), intraplaque hemorrhage (IPH), thin fibrous caps, plaque surface ulceration, huge dimension determining stenosis, and plaque rupture. Recognizing these macroscopic characteristics is crucial to estimating the risk of cerebrovascular events, also in case of non-significant (less than 50%) stenosis. Inflammatory biomarkers, such as cytokines and adhesion molecules, lipid-related markers like oxidized low-density lipoprotein (LDL), and proteolytic enzymes capable of degrading extracellular matrix components are among the key molecules that will be scrutinized for their associative roles in plaque instability. Through their quantification and evaluation, these biomarkers reveal intricate molecular cross-talking govern-ing plaque inflammation, rupture potential, and thrombogenicity. Current evidence demonstrates that plaque vulnerability phenotypes are multiple and heterogeneous and are associated with as many highly complex molecular pathways that determine the activation of an immune-mediated cascade that culminates in thromboinflammation. This narrative review provides a comprehen-sive analysis of current knowledge on molecular biomarkers expressed by symptomatic carotid plaques. It explores the association of these biomarkers with the structural and compositional at-tributes that characterize vulnerable plaques

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Section: Plaque Ulcerationmentioning

confidence: 99%

Molecular Pathways of Vulnerability Carotid Plaques at Risk for Ischemic Stroke: A Narrative Review

Miceli,

Basso,

Pintus

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…The study conducted by Loftus et al [51] on the expression of MMP-9 within this tissue demonstrated a significant increase in MMP-9 localized in the most unstable carotid plaques and the plaques of more symptomatic patients. Interestingly, MMP-9 has been considered an excellent candidate for future pharmacotherapy intended to stabilize carotid plaques and prevent stroke [89].…”

Section: Plaque Ulcerationmentioning

confidence: 99%

Molecular Pathways of Vulnerable Carotid Plaques at Risk of Ischemic Stroke: A Narrative Review

Miceli,

Basso,

Pintus

et al. 2024

IJMS

View full text Add to dashboard Cite

The concept of vulnerable carotid plaques is pivotal in understanding the pathophysiology of ischemic stroke secondary to large-artery atherosclerosis. In macroscopic evaluation, vulnerable plaques are characterized by one or more of the following features: microcalcification; neovascularization; lipid-rich necrotic cores (LRNCs); intraplaque hemorrhage (IPH); thin fibrous caps; plaque surface ulceration; huge dimensions, suggesting stenosis; and plaque rupture. Recognizing these macroscopic characteristics is crucial for estimating the risk of cerebrovascular events, also in the case of non-significant (less than 50%) stenosis. Inflammatory biomarkers, such as cytokines and adhesion molecules, lipid-related markers like oxidized low-density lipoprotein (LDL), and proteolytic enzymes capable of degrading extracellular matrix components are among the key molecules that are scrutinized for their associative roles in plaque instability. Through their quantification and evaluation, these biomarkers reveal intricate molecular cross-talk governing plaque inflammation, rupture potential, and thrombogenicity. The current evidence demonstrates that plaque vulnerability phenotypes are multiple and heterogeneous and are associated with many highly complex molecular pathways that determine the activation of an immune-mediated cascade that culminates in thromboinflammation. This narrative review provides a comprehensive analysis of the current knowledge on molecular biomarkers expressed by symptomatic carotid plaques. It explores the association of these biomarkers with the structural and compositional attributes that characterize vulnerable plaques.

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“…In addition, serum and plasma are readily available in most biobanks, thus saving time and effort in specimen collection and facilitating biomarker discovery. Consequently, the discovery of new diagnostic markers from serum and plasma is actively pursued worldwide [1][2][3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Proteome Analysis of Serum Purified Using Solanum tuberosum and Lycopersicon esculentum Lectins

Nakajima,

Konno,

Miyashita

et al. 2024

IJMS

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Serum and plasma exhibit a broad dynamic range of protein concentrations, posing challenges for proteome analysis. Various technologies have been developed to reduce this complexity, including high-abundance depletion methods utilizing antibody columns, extracellular vesicle enrichment techniques, and trace protein enrichment using nanobead cocktails. Here, we employed lectins to address this, thereby extending the scope of biomarker discovery in serum or plasma using a novel approach. We enriched serum proteins using 37 different lectins and subjected them to LC–MS/MS analysis with data-independent acquisition. Solanum tuberosum lectin (STL) and Lycopersicon esculentum lectin (LEL) enabled the detection of more serum proteins than the other lectins. STL and LEL bind to N-acetylglucosamine oligomers, emphasizing the significance of capturing these oligomer-binding proteins when analyzing serum trace proteins. Combining STL and LEL proved more effective than using them separately, allowing us to identify over 3000 proteins from serum through single-shot proteome analysis. We applied the STL/LEL trace-protein enrichment method to the sera of systemic lupus erythematosus model mice. This revealed differences in >1300 proteins between the systemic lupus erythematosus model and control mouse sera, underscoring the utility of this method for biomarker discovery.

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Searching for Atherosclerosis Biomarkers by Proteomics: A Focus on Lesion Pathogenesis and Vulnerability

Cited by 3 publications

References 184 publications

Molecular Pathways of Vulnerability Carotid Plaques at Risk for Ischemic Stroke: A Narrative Review

Molecular Pathways of Vulnerability Carotid Plaques at Risk for Ischemic Stroke: A Narrative Review

Molecular Pathways of Vulnerable Carotid Plaques at Risk of Ischemic Stroke: A Narrative Review

Proteome Analysis of Serum Purified Using Solanum tuberosum and Lycopersicon esculentum Lectins

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