Ameliorative Effects and Cellular Aspects of Phytoconstituents in Atherosclerosis

2020 ◽  
Vol 26 (22) ◽  
pp. 2574-2582
Author(s):  
Alamgeer ◽  
Hira Asif ◽  
Muhammad Z.A. Sandhu ◽  
Madiha Aziz ◽  
Hafiz M. Irfan ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Smooth Muscle ◽  
Molecular Mechanisms ◽  
Foam Cell ◽  
Current Knowledge ◽  
Preliminary Evidence ◽  
Plaque Formation ◽  
Atheromatous Plaque ◽  
Smooth Muscle Cell Migration ◽  
Pharmacological Studies

Atherosclerosis is a cardiovascular disease that involves vessels through the development of fatty streaks and plaques. Plant-based compounds can help treat or prevent atherosclerosis by affecting various factors that are involved in the disease. The present review discusses our current knowledge of the major cellular and molecular mechanisms of phytotherapeutics for the treatment of atherosclerosis. Numerous studies have evaluated the antiatherosclerotic activity of phytoconstituents to provide preliminary evidence of efficacy, but only a few studies have delineated the underlying molecular mechanisms. Plant-derived phytotherapeutics primarily targets abnormal levels of lipoproteins, endothelial dysfunction, smooth muscle cell migration, foam cell development, and atheromatous plaque formation. Nonetheless, the principal mechanisms that are responsible for their therapeutic actions remain unclear. Further pharmacological studies are needed to elucidate the underlying molecular mechanisms of the antiatherosclerotic response to these phytoconstituents.

scholarly journals Therapies for the Treatment of Cardiovascular Disease Associated with Type 2 Diabetes and Dyslipidemia

2021 ◽  
Vol 22 (2) ◽  
pp. 660
Author(s):  
María Aguilar-Ballester ◽  
Gema Hurtado-Genovés ◽  
Alida Taberner-Cortés ◽  
Andrea Herrero-Cervera ◽  
Sergio Martínez-Hervás ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Molecular Mechanisms ◽  
Foam Cell ◽  
Leukocyte Adhesion ◽  
Experimental Studies ◽  
Lipid Lowering ◽  
Foam Cell Formation ◽  
Relevant Parameter

Cardiovascular disease (CVD) is the leading cause of death worldwide and is the clinical manifestation of the atherosclerosis. Elevated LDL-cholesterol levels are the first line of therapy but the increasing prevalence in type 2 diabetes mellitus (T2DM) has positioned the cardiometabolic risk as the most relevant parameter for treatment. Therefore, the control of this risk, characterized by dyslipidemia, hypertension, obesity, and insulin resistance, has become a major goal in many experimental and clinical studies in the context of CVD. In the present review, we summarized experimental studies and clinical trials of recent anti-diabetic and lipid-lowering therapies targeted to reduce CVD. Specifically, incretin-based therapies, sodium-glucose co-transporter 2 inhibitors, and proprotein convertase subtilisin kexin 9 inactivating therapies are described. Moreover, the novel molecular mechanisms explaining the CVD protection of the drugs reviewed here indicate major effects on vascular cells, inflammatory cells, and cardiomyocytes, beyond their expected anti-diabetic and lipid-lowering control. The revealed key mechanism is a prevention of acute cardiovascular events by restraining atherosclerosis at early stages, with decreased leukocyte adhesion, recruitment, and foam cell formation, and increased plaque stability and diminished necrotic core in advanced plaques. These emergent cardiometabolic therapies have a promising future to reduce CVD burden.

scholarly journals Nuclear Transcription Factor Kappa B (NF-кB) and Molecular Damage Mechanisms in Acute Cardiovascular Diseases. A Review

2018 ◽  
Vol 4 (2) ◽  
pp. 65-72 ◽  
Author(s):  
Roxana Buzas ◽  
Alexandru Florin Rogobete ◽  
Sonia Elena Popovici ◽  
Tudor Mateescu ◽  
Teodora Hoinoiu ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Transcription Factor ◽  
Cardiovascular Diseases ◽  
Molecular Mechanisms ◽  
Severe Form ◽  
Molecular Therapy ◽  
Atheromatous Plaque ◽  
Early Evaluation ◽  
Nuclear Transcription Factor ◽  
Molecular Damage

Abstract Worldwide, cardiovascular diseases (CVDs) represent one of the main causes of morbidity and mortality, and acute coronary syndromes are responsible for a large number of sudden cardiac deaths. One of the main challenges that still exist in this area is represented by the early detection and targeted monitoring of the pathophysiology involved in CVDs. During the last couple of years, researchers have highlighted the importance of molecular and epigenetic mechanisms involved in the initiation and augmentation of CVDs, culminating in their most severe form represented by acute myocardial infarction. One of the most studied molecular factors involved in this type of pathology is represented by nuclear transcription factor kappa B (NF-κB), as well as the involvement of microRNAs (miRNAs). It has been suggested that miRNAs can also be involved in the complex process of atheromatous plaque vulnerabilization that leads to an acute cardiac event. In this review paper, we describe the most important molecular mechanisms involved in the pathogenesis of CVDs and atheromatous plaque progression and vulnerabilization, which include molecular mechanisms dependent on NF-κB. For this paper, we used international databases (PubMed and Scopus). The keywords used for the search were “miRNAs biomarkers”, “miRNAs in cardiovascular disease”, “NF-κB in cardiovascular disease”, “molecular mechanism in cardiovascular disease”, and “myocardial NF-κB mechanisms”. Numerous molecular reactions that have NF-κB as a trigger are involved in the pathogenesis of CVDs. Moreover, miRNAs play an important role in initiating and aggravating certain segments of CVDs. Therefore, miRNAs can be used as biomarkers for early evaluation of CVDs. Furthermore, in the future, miRNAs could be used as a targeted molecular therapy in order to block certain mechanisms responsible for inducing CVDs and leading to acute cardiovascular events.

scholarly journals Mechanisms of lead-induced hypertension and cardiovascular disease

2008 ◽  
Vol 295 (2) ◽  
pp. H454-H465 ◽  
Author(s):  
Nosratola D. Vaziri
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Disease ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Plasminogen Activator ◽  
Lead Exposure ◽  
Molecular Mechanisms ◽  
Subsequent Development ◽  
Endothelial Injury ◽  
Nitric Oxide Signaling

Lead is a ubiquitous environmental toxin that is capable of causing numerous acute and chronic illnesses. Population studies have demonstrated a link between lead exposure and subsequent development of hypertension (HTN) and cardiovascular disease. In vivo and in vitro studies have shown that chronic lead exposure causes HTN and cardiovascular disease by promoting oxidative stress, limiting nitric oxide availability, impairing nitric oxide signaling, augmenting adrenergic activity, increasing endothelin production, altering the renin-angiotensin system, raising vasoconstrictor prostaglandins, lowering vasodilator prostaglandins, promoting inflammation, disturbing vascular smooth muscle Ca2+ signaling, diminishing endothelium-dependent vasorelaxation, and modifying the vascular response to vasoactive agonists. Moreover, lead has been shown to cause endothelial injury, impede endothelial repair, inhibit angiogenesis, reduce endothelial cell growth, suppress proteoglycan production, stimulate vascular smooth muscle cell proliferation and phenotypic transformation, reduce tissue plasminogen activator, and raise plasminogen activator inhibitor-1 production. Via these and other actions, lead exposure causes HTN and promotes arteriosclerosis, atherosclerosis, thrombosis, and cardiovascular disease. In conclusion, studies performed in experimental animals, isolated tissues, and cultured cells have provided compelling evidence that chronic exposure to low levels of lead can cause HTN, endothelial injury/dysfunction, arteriosclerosis, and cardiovascular disease. More importantly, these studies have elucidated the cellular and molecular mechanisms of lead's action on cardiovascular/renal systems, a task that is impossible to accomplish using clinical and epidemiological investigations alone.

Di'ao Xinxuekang: Therapeutic Potential in Cardiovascular Diseases

2021 ◽  
Vol 14 ◽  
Author(s):  
Shengyu Zhang ◽  
Lingli Li ◽  
Mingying Deng ◽  
Yanan Wang ◽  
AiZong Shen ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Cardiovascular Diseases ◽  
Molecular Mechanisms ◽  
Blood Lipids ◽  
Clinical Decision Making ◽  
Therapeutic Potential ◽  
Clinical Decision ◽  
Pharmacological Effects ◽  
Herbal Preparation ◽  
Pharmacological Studies

Background: Cardiovascular disease is the leading cause of death in both developed and developing countries. Di'ao Xinxuekang (DAXXK) is a pure Chinese medicine herbal preparation refined from dioscin extracted from the roots of Dioscorea panthaica Prain et Burk and Diosorea nipponica Makino. Objective: To evaluate the application of DAXXK in Cardiovascular disease. Methods: : We searched and summarized all the studies on DAXXK and Cardiovascular disease in pumend, Google, and CNKI. Results: Modern pharmacological studies have shown that DAXXK has pharmacological effects such as dilating blood vessels, lowering blood pressure and cardiac load, improving hemodynamics, lowering blood lipids and anti-platelet aggregation, and is widely used for the therapy of various kinds of cardiovascular diseases, including hypertension, atherosclerosis, coronary heart disease (CHD), angina pectoris (AP) and myocardial infarction. We provide an overview of the clinical efficacy, molecular mechanisms, safety and therapeutic potential of DAXXK in the treatment of cardiovascular disease, aiming to provide clues and evidence for clinical decision-making. Conclusion: DAXXK exerts cardiovascular protection by regulating a variety of cardiovascular disease-related signaling pathways.

scholarly journals Targeting Platelet in Atherosclerosis Plaque Formation: Current Knowledge and Future Perspectives

2020 ◽  
Vol 21 (24) ◽  
pp. 9760
Author(s):  
Lei Wang ◽  
Chaojun Tang
Keyword(s):  
Risk Factors ◽  
Molecular Mechanisms ◽  
Vascular System ◽  
Current Knowledge ◽  
Vascular Inflammation ◽  
Plaque Formation ◽  
Inflammatory Factors ◽  
Future Perspectives ◽  
Atherosclerotic Plaque Formation

Besides their role in hemostasis and thrombosis, it has become increasingly clear that platelets are also involved in many other pathological processes of the vascular system, such as atherosclerotic plaque formation. Atherosclerosis is a chronic vascular inflammatory disease, which preferentially develops at sites under disturbed blood flow with low speeds and chaotic directions. Hyperglycemia, hyperlipidemia, and hypertension are all risk factors for atherosclerosis. When the vascular microenvironment changes, platelets can respond quickly to interact with endothelial cells and leukocytes, participating in atherosclerosis. This review discusses the important roles of platelets in the plaque formation under pro-atherogenic factors. Specifically, we discussed the platelet behaviors under disturbed flow, hyperglycemia, and hyperlipidemia conditions. We also summarized the molecular mechanisms involved in vascular inflammation during atherogenesis based on platelet receptors and secretion of inflammatory factors. Finally, we highlighted the studies of platelet migration in atherogenesis. In general, we elaborated an atherogenic role of platelets and the aspects that should be further studied in the future.

scholarly journals Macrophage Long Non-Coding RNAs in Pathogenesis of Cardiovascular Disease

2020 ◽  
Vol 6 (3) ◽  
pp. 28
Author(s):  
Marcin Wysoczynski ◽  
Jae Kim ◽  
Joseph B. Moore ◽  
Shizuka Uchida
Keyword(s):  
Cardiovascular Disease ◽  
Cell Fate ◽  
Foam Cell ◽  
Current Knowledge ◽  
Cell Formation ◽  
Foam Cell Formation ◽  
Macrophage Phenotype ◽  
Macrophage Function ◽  
Cell Fate Decisions ◽  
Non Coding Rnas

Chronic inflammation is inextricably linked to cardiovascular disease (CVD). Macrophages themselves play important roles in atherosclerosis, as well as acute and chronic heart failure. Although the role of macrophages in CVD pathophysiology is well-recognized, little is known regarding the precise mechanisms influencing their function in these contexts. Long non-coding RNAs (lncRNAs) have emerged as significant regulators of macrophage function; as such, there is rising interest in understanding how these nucleic acids influence macrophage signaling, cell fate decisions, and activity in health and disease. In this review, we summarize current knowledge regarding lncRNAs in directing various aspects of macrophage function in CVD. These include foam cell formation, Toll-like receptor (TLR) and NF-kβ signaling, and macrophage phenotype switching. This review will provide a comprehensive understanding concerning previous, ongoing, and future studies of lncRNAs in macrophage functions and their importance in CVD.

scholarly journals Is There a Link between COVID-19 Infection, Periodontal Disease and Acute Myocardial Infarction?

Life ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1050
Author(s):  
Ioana-Patricia Rodean ◽  
Carmen-Ioana Biriș ◽  
Vasile-Bogdan Halațiu ◽  
Andrei Modiga ◽  
Luminița Lazăr ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Periodontal Disease ◽  
Plaque Formation ◽  
Atheromatous Plaque ◽  
Tissue Destruction ◽  
Systemic Complications ◽  
Chronic Disorders ◽  
The Impact ◽  
Pro Inflammatory Cytokines

Both periodontal disease and atherosclerosis are chronic disorders with an inflammatory substrate that leads to alteration of the host’s immune response. In PD, inflammation is responsible for bone tissue destruction, while in atherosclerosis, it leads to atheromatous plaque formation. These modifications result from the action of pro-inflammatory cytokines that are secreted both locally at gingival or coronary sites, and systemically. Recently, it was observed that in patients with PD or with cardiovascular disease, COVID-19 infection is prone to be more severe. While the association between PD, inflammation and cardiovascular disease is well-known, the impact of COVID-19-related inflammation on the systemic complications of these conditions has not been established yet. The purpose of this review is to bring light upon the latest advances in understanding the link between periodontal–cardiovascular diseases and COVID-19 infection.

scholarly journals TLR4-mediated inflammation promotes foam cell formation of vascular smooth muscle cell by upregulating ACAT1 expression

2014 ◽  
Vol 5 (12) ◽  
pp. e1574-e1574 ◽  
Author(s):  
Y-W Yin ◽  
S-Q Liao ◽  
M-J Zhang ◽  
Y Liu ◽  
B-H Li ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Atherosclerotic Plaque ◽  
Proinflammatory Cytokines ◽  
Foam Cell ◽  
Cell Formation ◽  
Plaque Formation ◽  
Foam Cell Formation ◽  
Atherosclerotic Plaque Formation

Abstract Vascular smooth muscle cell (VSMC) foam cell formation is an important hallmark, especially in advanced atherosclerosis lesions. Acyl-coenzyme A:cholesterol acyltransferase 1 (ACAT1) promotes foam cell formation by promoting intracellular cholesteryl ester synthesis. The present study tests the hypothesis that oxidized low-density lipoprotein (oxLDL) increases the ACAT1 expression by activating the Toll-like receptor 4 (TLR4)-mediated inflammation, and ultimately promotes VSMC foam cell formation. Wild-type, ApoE−/−, TLR4−/− and ACAT1−/− mice on a C57BL/6J background were used. Increased TLR4, proinflammatory cytokines and ACAT1 were observed in high-fat (HF) diet-induced atherosclerotic plaque formation and in oxLDL-stimulated VSMCs. ACAT1 deficiency impeded the HF diet-induced atherosclerotic plaque formation and impaired the TLR4-manipulated VSMC foam cell formation in response to oxLDL. TLR4 deficiency inhibited the upregulation of myeloid-differentiating factor 88 (MyD88), nuclear factor-κB (NF-κB), proinflammatory cytokines and ACAT1, and eventually attenuated the HF diet-induced atherosclerotic plaque formation and suppressed the oxLDL-induced VSMC foam cell formation. Knockdown of MyD88 and NF-κB, respectively, impaired the TLR4-manipulated VSMC foam cell formation in response to oxLDL. Rosiglitazone (RSG) attenuated HF diet-induced atherosclerotic plaque formation in ApoE−/− mice, accompanied by reduced expression of TLR4, proinflammatory cytokines and ACAT1 accordingly. Activation of peroxisome proliferator-activated receptor γ (PPARγ) suppressed oxLDL-induced VSMC foam cell formation and inhibited the expression of TLR4, MyD88, NF-κB, proinflammatory cytokines and ACAT1, whereas inhibition of PPARγ exerted the opposite effect. TLR4−/− mice and VSMCs showed impaired atherosclerotic plaque formation and foam cell formation, and displayed no response to PPARγ manipulation. In conclusion, our data showed that oxLDL stimulation can activate the TLR4/MyD88/NF-κB inflammatory signaling pathway in VSMCs, which in turn upregulates the ACAT1 expression and finally promotes VSMC foam cell formation.

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