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The Interplay Between LIPCAR, Cuproptosis, and Α-SMA in the Pathogenesis of Acute Myocardial Infarction and Remodeling
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
Details
| Lead sponsor | Assiut University |
|---|---|
| Status | NOT_YET_RECRUITING |
| Enrolment | 50 |
| Start date | 2025-03 |
| Completion | 2027-07 |
Conditions
- Acute Myocardial Infarction (AMI)
Interventions
- blood sampling
Primary outcomes
- 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 — 2 years
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). - 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 — 2 years
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.