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NOT YET RECRUITING
NCT06833918

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

Sponsor: Assiut University

View on ClinicalTrials.gov

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

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).