Genetics of adrenergic signaling drives coronary artery calcification

Gambardella, Jessica; Wang, Xujun; Mone, Pasquale; Khondkar, Wafiq; Santulli, Gaetano

doi:10.1016/j.atherosclerosis.2020.07.025

Cited by 17 publications

(13 citation statements)

References 25 publications

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“…A high-quality randomized controlled trial with larger sample size and longer follow-up should be performed to clarify these results as well as evaluate the costeffectiveness of TMZ. Acute myocardial infarction (AMI) is a common cardiovascular disease that causes tissue damage, triggers a series of inflammatory processes, and even results in death [25]. Events, such as endothelial injury, that can lead to a hyperactive and pr-inflammatory phenotype of endothelial cells, first cause coronary atherosclerotic heart disease [25].…”

Section: Discussionmentioning

confidence: 99%

“…Acute myocardial infarction (AMI) is a common cardiovascular disease that causes tissue damage, triggers a series of inflammatory processes, and even results in death [25]. Events, such as endothelial injury, that can lead to a hyperactive and pr-inflammatory phenotype of endothelial cells, first cause coronary atherosclerotic heart disease [25]. CRP and TNF-α are some early markers of inflammation and tissue damage [26][27][28][29][30].…”

Section: Discussionmentioning

confidence: 99%

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Assessment of Trimetazidine Treatment in Acute Myocardial Infarction Patients Undergoing Percutaneous Coronary Intervention

Tang

Gong

2022

Cardiology Research and Practice

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Aims. Trimetazidine (TMZ) is effective at improving clinical outcomes in chronic heart failure and stable coronary artery disease patients. However, no single study has comprehensively evaluated the efficacy of TMZ in acute myocardial infarction (AMI) patients undergoing percutaneous coronary intervention (PCI). Methods. We enrolled 401 Chinese patients. All patients received the same drug prescription except for TMZ. In blinded fashion, patients were randomized to either a control or an experimental group in which 60 mg TMZ was provided at admission and then at 20 mg three times a day thereafter. At 2 and/or 6 days, we evaluated creatine kinase (CK and CK-MB), cardiac troponin I (cTnI), C-reaction protein (CRP), serum tumor necrosis factor (TNF-α), serum creatinine (Cr), serum urea, glucose, glutamic pyruvic transaminase (ALT), and glutamic oxaloacetic transaminase (AST). Additionally, by echocardiography, we assessed left ventricular ejection fraction (LVEF), left ventricular end-diastolic dimension (LVEDD), and cardiac output (CO). Results. CK and CKMB, which were recorded on the second day in the hospital (each p = 0.022 ), and cTNI, which was recorded on the sixth day in the hospital ( p = 0.003 ), were reduced with TMZ treatment compared to control. In addition, ALT and AST ( p = 0.001 , p = 0.000 , respectively) and glucose after 6 days ( p = 0.011 ) were significantly lower in the study group than in the control group. Furthermore, LVEF after 10–14 days and 6 months after discharge ( p = 0.039 and p = 0.047 , respectively) was increased with TMZ treatment. The effects of TMZ on CRP, TNF-α, Cr, urea, LVEDD, and CO were not significant (all p > 0.05 ). Conclusions. For AMI patients undergoing PCI, TMZ reduced circulating biomarkers of myocardial infarction, reduced values of ALT, AST, and glucose, and improved cardiac function compared with the control group.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Assessment of Trimetazidine Treatment in Acute Myocardial Infarction Patients Undergoing Percutaneous Coronary Intervention

Tang

Gong

2022

Cardiology Research and Practice

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“…TNF ligand-related molecule 1A inhibits vascular calcification by inhibiting osteogenic differentiation [ 43 ]. Moreover, the G protein signaling pathway could be implicated in the osteogenic differentiation of VSMCs during vascular calcification [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Liver kinase B1 inhibits smooth muscle calcification via high mobility group box 1

Zhang

Chen

et al. 2021

Redox Biology

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Vascular calcification is a common pathological feature of atherosclerosis, chronic kidney disease, vascular injury, and aging. Liver kinase B1 (LKB1) plays pivotal roles in cellular processes such as apoptosis, metabolism, and cell cycle regulation. In addition, growing evidence has indicated that LKB1 functions as a tumor suppressor gene. However, its role in vascular calcification has not been reported. LKB1 flox/flox mice were hybridized with SM22-CreER T2 transgenic mice and adult mice received tamoxifen to obtain smooth muscle-specific LKB1-knockout (LKB1 SMKO ) mice. LKB1 expression was decreased under calcifying conditions, and LKB1 overexpression had a protective effect on vascular calcification. However, high mobility group box 1 (HMGB1) overexpression partially counteracted the promotion of vascular calcification induced by LKB1 overexpression. Mechanically, LKB1 could bind to HMGB1 to promote HMGB1 degradation. Furthermore, LKB1 SMKO mice showed intensified vascular calcification, which was alleviated by treatment with the HMGB1 inhibitor glycyrrhizic acid. Based on our results, LKB1 may inhibit vascular calcification via inhibiting HMGB1 expression.

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“… 28 This association may be more related to the plaque’s contents (i.e., degree of calcification) than its size. 29 , 30 There are several direct hemodynamic consequences of increased PWV. For one, age-related widening of PP—the difference between systolic and diastolic blood pressure—is partly determined by arterial stiffening.…”

Section: How To Quantify Arterial Stiffness?mentioning

confidence: 99%

Chronic kidney disease: Definition, updated epidemiology, staging, and mechanisms of increased cardiovascular risk

Wilson

Mone

Jankauskas

et al. 2021

J of Clinical Hypertension

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Chronic kidney disease (CKD) is a heterogeneous group of disorders that manifest in various ways depending upon the severity of disease and the underlying cause(s). 1 | CK D: DEFINITI ONChronic kidney disease is defined by the presence of kidney damage or decreased kidney function for at least three months, irrespective of the cause. 2 Kidney damage generally refers to pathologic anomalies in the native or transplanted kidney, established via imaging, biopsy, or deduced from clinical markers like increased albuminuria-that is, albumin-to-creatinine ratio (ACR) >30 mg/g (3.4 mg/mMol)-or urinary sediment alterations; decreased kidney function refers to a reduced glomerular filtration rate (GFR), which is usually estimated (eGFR) from the serum concentration of creatinine. 3 | UPDATED CK D EPIDEMI OLOGYAccording to the US Centers for Disease Control and Prevention (CDC), ~37 million people in the United States-~15% of adults-are estimated to have CKD. Of note, 90% of adults with CKD do not know they have it and 1 in 2 people with very low kidney function who are not on dialysis are not aware of the fact that they have CKD. 4 Diabetes and hypertension are the major causes of CKD in adults: According to the CDC, 1 in 3 adults with diabetes and 1 in 5 adults with hypertension may have CKD. According to the current CDC statistics, CKD is more common in people aged 65 years or older (38%) than in people aged 45-64 years (13%) or 18-44 years (7%), and is slightly more common in women (15%) than men (12%); moreover, African Americans are about 3 times more likely than whites to develop ESKD. 5

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Genetics of adrenergic signaling drives coronary artery calcification

Cited by 17 publications

References 25 publications

Assessment of Trimetazidine Treatment in Acute Myocardial Infarction Patients Undergoing Percutaneous Coronary Intervention

Assessment of Trimetazidine Treatment in Acute Myocardial Infarction Patients Undergoing Percutaneous Coronary Intervention

Liver kinase B1 inhibits smooth muscle calcification via high mobility group box 1

Chronic kidney disease: Definition, updated epidemiology, staging, and mechanisms of increased cardiovascular risk

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