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LIPCAR, Cuproptosis, and Α-SMA in the Pathogenesis of AMI and Remodeling

NCT06833918 · Status: NOT_YET_RECRUITING · Type: OBSERVATIONAL · Enrollment: 50

Last updated 2025-02-19

No results posted yet for this study

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

Conditions

  • Acute Myocardial Infarction (AMI)

Interventions

GENETIC

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).

Sponsors & Collaborators

  • Assiut University

    lead OTHER

Eligibility

Sex
ALL
Healthy Volunteers
Yes

Timeline & Regulatory

Start
2025-03-31
Primary Completion
2027-01-31
Completion
2027-07-31

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Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT06833918 on ClinicalTrials.gov