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LIPCAR, Cuproptosis, and Α-SMA in the Pathogenesis of AMI and Remodeling
Sponsor: Assiut University
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
Official title: The Interplay Between LIPCAR, Cuproptosis, and Α-SMA in the Pathogenesis of Acute Myocardial Infarction and Remodeling
Key Details
Gender
All
Age Range
Any - Any
Study Type
OBSERVATIONAL
Enrollment
50
Start Date
2025-03
Completion Date
2027-07
Last Updated
2025-02-19
Healthy Volunteers
Yes
Conditions
Interventions
blood sampling
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).