C-reactive protein is released in the coronary circulation and causes endothelial dysfunction in patients with acute coronary syndromes

Forte, L. A.; Cimmino, Giovanni; Loffredo, Francesco; Palma, Raffaele De; Abbate, Gianfranco; Calabrò, Paolo; Ingrosso, Diego; Galletti, Patrizia; Carangio, Ciro; Casillo, Beniamino; Calabrò, Raffaele; Golino, Paolo

doi:10.1016/j.ijcard.2011.05.062

Cited by 40 publications

(25 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These data have been confirmed by the discovery that CRP may be released not only from hepatocytes but also from other different cell types [39-41]. Taken together with previous observation from our group and others [38, 42, 43], regarding the active production of CRP within the coronary circulation of ACS patients and in cerebrovascular patients, the main question raised was related to the possible local effects exerted by CRP on the different cellular components of the atherosclerotic lesion. By biological and molecular point of view, CRP may promote endothelial function inducing adhesion molecules [44-47], favouring a pro-atherogenic phenotype via expression of TF [48], releasing MCP-1 [49] and other inflammatory cytokines [50, 51], increasing iNOS and superoxide production and decreasing eNOS, prostacyclin and tPA expression in endothelial cells [45, 52].…”

Section: Inflammatory Side Of Atherosclerosis:systemic Vs Local Inflsupporting

confidence: 83%

“…However, despite the emerging role of CRP and other inflammatory mediators as systemic prognostic markers, more recent studies have focused on the “inflammatory status” at the site of atherosclerotic plaque as major determinant in plaque destabilization [8, 38]. These data have been confirmed by the discovery that CRP may be released not only from hepatocytes but also from other different cell types [39-41].…”

Section: Inflammatory Side Of Atherosclerosis:systemic Vs Local Inflmentioning

confidence: 99%

See 1 more Smart Citation

Immune-Inflammatory Activation in Acute Coronary Syndromes: A Look into the Heart of Unstable Coronary Plaque

Cimmino

Loffredo

Morello

et al. 2017

CCR

Self Cite

View full text Add to dashboard Cite

In the last twenty years, our comprehension of the molecular mechanisms involved in the formation, progression and complication of atherosclerotic plaque has advanced significantly and the main role of inflammation and immunity in this phenomenon is now largely accepted. Accumulating evidence highlight the crucial role of different inflammatory and immune cells, such as monocytes and T-lymphocytes, in the pathophysiology of atherosclerotic lesion, particularly in contributing to its com-plications, such as rupture or ulceration. According to the new terminology, “vulnerable plaque” identi-fies an inflamed atherosclerotic lesion that is particularly prone to rupture. Once disrupted, prothrom-botic material is exposed to the flowing blood, thus activating coagulation cascade and platelet aggrega-tion, ultimately leading to acute thrombus formation within the coronary vessel. To date this is the key event underlying the clinical manifestations of acute coronary syndromes (ACS).The degree of vessel occlusion (complete vs. incomplete) and the time of blood flow cessation will define the severity of clinical picture. This phenomenon seems to be the final effect of a complex inter-action between different local and systemic factors, involving the degree of inflammation, type of cells infiltration and the rheological characteristics of blood flow at the site of plaque rupture, thrombogenic substrates within the atherosclerotic lesion and different soluble mediators, already present or acutely released in the circulating blood. This article will review currently available data on the pathophysiology of ACS, emphasizing the immunological and inflammatory aspects of vulnerable plaque. We may pos-tulate that intraplaque antigens and local microenvironment will define the immune-inflammatory re-sponse and cells phenotype, thus determining the severity of clinical manifestations.

show abstract

Section: Inflammatory Side Of Atherosclerosis:systemic Vs Local Inflsupporting

confidence: 83%

Section: Inflammatory Side Of Atherosclerosis:systemic Vs Local Inflmentioning

confidence: 99%

Immune-Inflammatory Activation in Acute Coronary Syndromes: A Look into the Heart of Unstable Coronary Plaque

Cimmino

Loffredo

Morello

et al. 2017

CCR

Self Cite

View full text Add to dashboard Cite

show abstract

“…CRP induces ECs to express various adhesion molecules and chemotactic molecules. CRP also stimulates monocytes to produce and secrete potent pro-coagulant factors promoting the inflammatory response (130, 131). Plasminogen activator inhibitor-1 (PAI-1) is a major inhibitor for fibrinolysis and an important risk factor for thrombotic diseases (132).…”

Section: Function Of Mscs In Atherosclerosismentioning

confidence: 99%

Function and Therapeutic Potential of Mesenchymal Stem Cells in Atherosclerosis

Guo

Chen

2017

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

Atherosclerosis is a complicated disorder and largely attributable to dyslipidaemia and chronic inflammation. Despite therapeutic advances over past decades, atherosclerosis remains the leading cause of mortality worldwide. Due to their capability of immunomodulation and tissue regeneration, mesenchymal stem cells (MSCs) have evolved as an attractive therapeutic agent in various diseases including atherosclerosis. Accumulating evidences support the protective role of MSCs in all stages of atherosclerosis. In this review, we highlight the current understanding of MSCs including their characteristics such as molecular markers, tissue distribution, migratory property, immune-modulatory competence, etc. We also summarize MSC functions in animal models of atherosclerosis. MSC transplantation is able to modulate cytokine and chemokine secretion, reduce endothelial dysfunction, promote regulatory T cell function, decrease dyslipidemia, and stabilize vulnerable plaques during atherosclerosis development. In addition, MSCs may migrate to lesions where they develop into functional cells during atherosclerosis formation. Finally, the perspectives of MSCs in clinical atherosclerosis therapy are discussed.

show abstract

“…In most cells and situations, the role of the Na + /Ca 2 + exchanger is to remove Ca 2 + from the cell (forward mode); however, under some conditions the exchanger can mediate the net influx of Ca 2 + (reverse mode). Recent studies have shown that abnormal Na + /Ca 2 + exchanger activation contributes to both diabetic micro-and macroangiopathy The endothelium is the common target of all cardiovascular risk factors, and functional impairment of the vascular endothelium in response to injury occurs long before the development of visible atherosclerosis (Forte et al, 2011). Decreased nitric oxide production, increased oxidative stress and impaired function of endothelial progenitor cells are the main mechanisms involved in the accelerated atherosclerotic process observed in diabetes mellitus patients (Fidan et al, 2011).…”

Section: Effects Of the Na + /Ca 2 + Exchanger Inhibitor On Biochemicmentioning

confidence: 99%

Na+/Ca2+ Exchanger Inhibitor Restores Endothelium-dependent Relaxation in Diabetic Rat Aorta

Wan

Sun

et al. 2015

Exp Clin Endocrinol Diabetes

View full text Add to dashboard Cite

The aims of this study were to examine the effects of KB-R7943, an inhibitor of Na(+)/Ca(2+) exchanger, on the endothelium-dependent relaxation (EDR) in diabetic rat aorta. Both acetylcholine (ACh)-induced EDR and sodium nitroprusside (SNP)-induced endothelium-independent relaxation (EIR) were measured in aortic rings of nondiabetic and streptozotocin-diabetic rats. Diabetes mellitus was induced by single injection of streptozotocin (60 mg/kg). The treated rats received 0.01 or 0.1 mg/kg/day of KB-R7943 for 8 weeks. ACh-induced relaxation was impaired in diabetic compared to control rings and the vasodilatation to SNP was unaffected. Treatment with KB-R7943 markedly enhanced relaxation to ACh in diabetic but not in control rings. KB-R7943 significantly increased superoxide dismutase (SOD) activity and the nitric oxide (NO) release. These results suggest that KB-R7943 can restore impaired EDR in aortic rings of diabetic rats, which may be related to scavenging oxygen free radicals and enhancing NO production.

show abstract

C-reactive protein is released in the coronary circulation and causes endothelial dysfunction in patients with acute coronary syndromes

Cited by 40 publications

References 33 publications

Immune-Inflammatory Activation in Acute Coronary Syndromes: A Look into the Heart of Unstable Coronary Plaque

Immune-Inflammatory Activation in Acute Coronary Syndromes: A Look into the Heart of Unstable Coronary Plaque

Function and Therapeutic Potential of Mesenchymal Stem Cells in Atherosclerosis

Na+/Ca2+ Exchanger Inhibitor Restores Endothelium-dependent Relaxation in Diabetic Rat Aorta

Contact Info

Product

Resources

About