Pathophysiology and mechanisms of Acute Coronary Syndromes: atherothrombosis, immune-inflammation, and beyond

Cimmino, Giovanni; Serafino, Luigi Di; Cirillo, Plinio

doi:10.1080/14779072.2022.2074836

Cited by 14 publications

(8 citation statements)

References 157 publications

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“…The final effect of UA in inducing ED and inflammation, through all the pathways already indicated above, is a procoagulant state that might result in vascular thrombosis [133]. The link between ED, inflammation and thrombosis is well known [113,134].…”

Section: Ua and Prothrombotic Statementioning

confidence: 98%

Uric acid in atherosclerosis and cardiovascular diseases: innocent bystander or ruthless killer?

Cimmino,

Natale,

Franzese

et al. 2024

Explor Musculoskeletal Dis

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Medical attention to uric acid (UA) has been increasing in recent years, mainly because this molecule has been shown to be associated with increased cardiovascular risk, both in the general population and in the hypertensive patients. A growing body of clinical and experimental data supports this view and prompts reconsideration of the role of UA in the development of atherosclerosis and the genesis of cardiovascular disease. It is known that this substance, in certain plasma concentrations, induces increased oxidative stress, a chronic inflammatory state, and a whole series of other modifications that are potentially deleterious at the cardiovascular level leading to hypertension, atherosclerosis, atrial fibrillation (AF), and other metabolic changes such as diabetes, metabolic syndrome, non-alcoholic fatty liver disease and kidney failure. Despite this epidemiologic and mechanistic evidence, the current guidelines from international cardiology scientific societies do not give precise indications in this regard, and some of them only suggest UA evaluation as part of an initial screening of the hypertensive patient. The purpose of this review is to briefly describe the main clinical and epidemiological evidence supporting the role of hyperuricemia as a possible emerging cardiovascular risk factor and to analyze the potential pathophysiological mechanisms through which elevated UA levels may exert a detrimental effect on the cardiovascular system.

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Section: Ua and Prothrombotic Statementioning

confidence: 98%

Uric acid in atherosclerosis and cardiovascular diseases: innocent bystander or ruthless killer?

Cimmino,

Natale,

Franzese

et al. 2024

Explor Musculoskeletal Dis

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“…Platelets and inflammatory cells secrete growth factors, such as fibroblast growth factor 2 (FGF-2), epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and insulin-like growth factor (IGF). These growth factors are responsible for initiating vascular smooth muscle cells (VSMCs) proliferation through tyrosine kinase receptors [ 16 17 ]. VSMCs switch from a quiescent contractile phenotype to a synthetic phenotype and migrate to the intima.…”

Section: Vascular Response To Endovascular Interventionmentioning

confidence: 99%

A review of the current state in neointimal hyperplasia development following endovascular intervention and minor emphasis on new horizons in immunotherapy

Dinc

2023

Transl Clin Pharmacol

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Endovascular strategies play a vital role in the treatment of peripheral arterial disease (PAD). However, luminal loss or restenosis after endovascular intervention remains a significant challenge. The main underlying mechanisms are negative vascular remodeling and elastic recoil in balloon angioplasty. During stenting, the main reason for this complex is neointimal proliferation. Endothelial cell injury due to endovascular intervention initiates a series of molecular events, such as overexpression of growth factors, cytokine secretion, and adhesion molecules. These induce platelet activation and inflammatory processes, which trigger the proliferation and migration of vascular smooth muscle cells into the intima, resulting in neointimal hyperplasia. During this process, PAD progression is mainly caused by chronic inflammation, in which macrophages play a central role. Of the current strategies, drug release interventions aim to suppress restenosis using antiproliferative drugs, such as sirolimus and paclitaxel, during drug release. These drugs inhibit vascular reendothelialization and reduce late in-stent restenosis. For this reason, immunotherapy can be considered an important alternative. Interventions that polarize macrophages to the M2 subtype are particularly important, as they shape the immune response in an anti-inflammatory direction and contribute to tissue repair. However, there are several challenges to overcome, such as localizing antiproliferative or polarizing agents only to areas of vascular injury. This review discusses, based on the early study observations, immunotherapeutic approaches to prevent restenosis after endovascular intervention for the treatment of PAD.

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“…The foremost common cause of thrombosis is the rupture of vulnerable plaques. It has been established that the characteristics of vulnerable plaques include massive monocyte/macrophage infiltration, bulky lipid-rich necrotic cores, thin fibrous caps, and fewer SMCs [ 92 ]. Macrophages under the fibrous cap can reduce ECMs by their phagocytic function.…”

Section: Ferroptosis Involvement In the Pathological Progression Of Chdmentioning

confidence: 99%

From Iron Metabolism to Ferroptosis: Pathologic Changes in Coronary Heart Disease

Fan

Yan

et al. 2022

Oxidative Medicine and Cellular Longevity

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Coronary heart disease (CHD) is closely related to oxidative stress and inflammatory response and is the most common cardiovascular disease (CVD). Iron is an essential mineral that participates in many physiological and biochemical reactions in the human body. Meanwhile, on the negative side, iron has an active redox capacity, which leads to the accumulation of reactive oxygen species (ROS) and lipid peroxidation. There is growing evidence that disordered iron metabolism is involved in CHD’s pathological progression. And the result of disordered iron metabolism is associated with iron overload-induced programmed cell death, often called ferroptosis. That features iron-dependent lipid peroxidation. Ferroptosis may play a crucial role in the development of CHD, and targeting ferroptosis may be a promising option for treating CHD. Here, we review the mechanisms of iron metabolism in cardiomyocytes (CMs) and explain the correlation between iron metabolism and ferroptosis. Meanwhile, we highlight the specific roles of iron metabolism and ferroptosis in the main pathological progression of CHD.

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Pathophysiology and mechanisms of Acute Coronary Syndromes: atherothrombosis, immune-inflammation, and beyond

Cited by 14 publications

References 157 publications

Uric acid in atherosclerosis and cardiovascular diseases: innocent bystander or ruthless killer?

Uric acid in atherosclerosis and cardiovascular diseases: innocent bystander or ruthless killer?

A review of the current state in neointimal hyperplasia development following endovascular intervention and minor emphasis on new horizons in immunotherapy

From Iron Metabolism to Ferroptosis: Pathologic Changes in Coronary Heart Disease

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