LIPCAR, Cuproptosis, and Α-SMA in the Pathogenesis of AMI and Remodeling
The Interplay Between LIPCAR, Cuproptosis, and Α-SMA in the Pathogenesis of Acute Myocardial Infarction and Remodeling
1 other identifier
observational
50
0 countries
N/A
Brief Summary
The pathophysiology of acute myocardial infarction is multifaceted, involving numerous biological processes. The crosstalk between cuproptosis and remodeling biomarkers may be implicated in the pathogenesis of AMI. Combining cuproptosis, LIPCAR, and α-SMA cardiac recovery analysis may enable more precise identification of diagnostic biomarkers that help for future improvement of treatment and prognosis
Trial Health
Trial Health Score
Automated assessment based on enrollment pace, timeline, and geographic reach
participants targeted
Target at P25-P50 for all trials
Started Mar 2025
Typical duration for all trials
Health score is calculated from publicly available data and should be used for screening purposes only.
Trial Relationships
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Study Timeline
Key milestones and dates
First Submitted
Initial submission to the registry
January 13, 2025
CompletedFirst Posted
Study publicly available on registry
February 19, 2025
CompletedStudy Start
First participant enrolled
March 1, 2025
CompletedPrimary Completion
Last participant's last visit for primary outcome
January 1, 2027
ExpectedStudy Completion
Last participant's last visit for all outcomes
July 1, 2027
February 19, 2025
January 1, 2025
1.8 years
January 13, 2025
February 13, 2025
Conditions
Outcome Measures
Primary Outcomes (2)
The present study will include two groups: First group: 50 AMI patients and Second group (control): 50 age and gender matched healthy volunteers without history of pre-existing or existing cardiovascular comorbidities with normal cardiac enzymes
The followings markers will be investigated in plasma samples: 1. LIPCAR, STAT3 and DDIT3 using quantitative real-time polymerase chain reaction (qRT-PCR) 2. α-SMA using western blot analysis 3. Troponin T using ELISA expression 4. Serum levels of fasting blood glucose (FBG), total cholesterol (TC), triglycerides (TG), and high-density lipoprotein cholesterol (HDL-C), oxidized low-density lipoprotein (ox-LDL) using chemical methods (spectrophotometry). The Friedewald formula will be used to compute low-density lipoprotein cholesterol (LDL-C): LDL-Cholesterol =Total cholesterol- (HDL-Cholesterol +Triglycerides/5).
2 years
AMI is a myocardial injury event induced by rupture of atherosclerotic plaques and thrombosis. Rapid and accurate identification of AMI in accordance with reducing myocardial cell death has become a critical component for early diagnosis and improvement
The followings markers will be investigated in plasma samples using quantitative real-time polymerase chain reaction (qRT-PCR): 1. LIPCAR, 2. STAT3, 3. DDIT3, 4. α-SMA and 5. Troponin T * To measure LIPCAR, STAT3 and DDIT3 expression in AMI patients for identifying their role in the pathogenesis of AMI, that could enable further research on its role as a potential therapeutic target. * To detect the relationship between LIPCAR, STAT3 and DDIT3 expression and Age, gender, BMI, diabetes mellitus (DM), hypertension (HTN), dyslipidaemia,smoking, and obesity. * To detect the relationship between α-SMA protein expression and cardiac regeneration and repair, so that healthcare providers can make more informed decisions regarding treatment strategies, allowing for tailored pharmacological or intervention approaches based on individual patient needs and significantly enhancing heart function and improving the overall quality of life for patients recovering from myocardial infarction.
2 years
Interventions
The followings markers will be investigated in plasma samples: 1. LIPCAR, STAT3 and DDIT3 using quantitative real-time polymerase chain reaction (qRT-PCR) 2. α-SMA using western blot analysis 3. Troponin T using ELISA expression 4. Serum levels of fasting blood glucose (FBG), total cholesterol (TC), triglycerides (TG), and high-density lipoprotein cholesterol (HDL-C), oxidized low-density lipoprotein (ox-LDL) using chemical methods (spectrophotometry). The Friedewald formula was used to compute low-density lipoprotein cholesterol (LDL-C): LDL-Cholesterol =Total cholesterol- (HDL-Cholesterol +Triglycerides/5).
Eligibility Criteria
The present study will include 50 AMI patients diagnosed and screened based on criteria including persistent chest pain, electrocardiogram changes, and high-sensitivity cardiac troponin I (cTnI) and T testing during their hospital admission to the cardiac catheter unit, department of cardiology, faculty of medicine, Assiut university hospital. Patient features will be anonymously analysed in addition to 50 age and gender matched healthy volunteers without history of cardiovascular diseases or other organ issues, no pre-existing or existing cardiovascular symptoms like chest pain during their routine physical examinations in the hospital, normal cardiac enzyme cTnI and T levels, coronary artery stenosis \<50% on coronary angiography, and normal ECG parameters as a control group
You may qualify if:
- All patients will be subjected to full history taking, meticulous general examination, and local cardiac examination
- Age ≥ 18 years
- AMI diagnosis : clinical, laboratory (troponins level), ECG and coronary angiography indicated occlusion or (≥50% stenosis of any coronary artery or its major branches)
You may not qualify if:
- Patients with aortic coarctation,
- Coronary artery bypass grafting surgery,
- Coronary intervention,
- Congestive heart failure,
- Rheumatic heart disease,
- Presence of coronary myocardial bridges,
- Organic cardiac disease such as combined heart valve disease,
- Congenital heart defects,
- Any inflammatory diseases like myocarditis or pericarditis, traumatic cardiac injury or other primary heart diseases,
- Dilated cardiomyopathy,
- Hypertrophic cardiomyopathy,
- Patients complicated with malignant arrhythmias.
- Patients with severe haematological disease,
- Infection as tuberculosis,
- Pulmonary embolism,
- +7 more criteria
Contact the study team to confirm eligibility.
Sponsors & Collaborators
Biospecimen
Blood Sample Collection For plasma isolation a total of 5 ml of peripheral antecubital venous blood will be obtained in the morning after an overnight fast from each patient within 24 h of the onset of myocardial infarction and from healthy controls in EDTA-containing tubes. The plasma will be separated by centrifugation at 800 g for 10 min. The supernatant plasma samples will be divided into RNase-free Eppendorf tubes and stored at - 80 until analysis.
MeSH Terms
Interventions
Intervention Hierarchy (Ancestors)
Central Study Contacts
Study Design
- Study Type
- observational
- Observational Model
- CASE CONTROL
- Time Perspective
- PROSPECTIVE
- Target Duration
- 6 Months
- Sponsor Type
- OTHER
- Responsible Party
- PRINCIPAL INVESTIGATOR
- PI Title
- Dr
Study Record Dates
First Submitted
January 13, 2025
First Posted
February 19, 2025
Study Start
March 1, 2025
Primary Completion (Estimated)
January 1, 2027
Study Completion (Estimated)
July 1, 2027
Last Updated
February 19, 2025
Record last verified: 2025-01