Role of Serum Endothelin-Converting Enzyme-1 (ECE-1), Adenosine Monophosphate-Activated Protein Kinase (AMPK), and Oxidized Low-Density Lipoprotein (Ox-LDL) in the Pathophysiology and Theoretical Diagnostic Framework of Type 2 Diabetic Mellitus Patients w

الملخص

Background: Type 2 diabetes mellitus (T2DM) significantly increases the risk of acute myocardial infarction (AMI) through mechanisms including vascular dysfunction, oxidative stress, and inflammation. Conventional diagnostic tools, such as electrocardiography and troponins, often exhibit limited efficacy in patients with T2DM due to atypical symptom presentation.

Materials and Methods: This narrative review synthesizes published evidence from basic, preclinical, and clinical studies on the structure, functions, and interplay of a panel of serum biomarkers — endothelin-converting enzyme-1 (ECE-1), adenosine monophosphate-activated protein kinase (AMPK), and oxidized low-density lipoprotein (ox-LDL) — in the pathophysiology of AMI in the context of T2DM (T2DM-AMI). This narrative review synthesizes published evidence from basic, preclinical, and clinical studies on the structure, functions, and interplay of a panel of serum biomarkers — ECE-1, AMPK, and ox-LDL — in the pathophysiology of AMI in the context of T2DM (T2DM-AMI). No original patient data, clinical cohorts, or laboratory measurements are presented. The diagnostic potential discussed is derived from mechanistic and correlational studies and remains theoretical.

Results: ECE-1 promotes vasoconstriction via endothelin-1 (ET-1), AMPK serves as a master regulator of cellular energy balance, and ox-LDL is a key driver of atherosclerosis. Their interactions highlight a vicious cycle of metabolic and vascular damage. Based on published mechanistic and correlational evidence, combining these biomarkers may theoretically improve early diagnosis and personalized treatment; however, this remains hypothetical pending clinical validation in prospective cohorts containing original patient data. No quantitative diagnostic metrics (sensitivity, specificity, AUC-ROC, or cutoff thresholds) for the proposed biomarker panel are available from the current literature. Similarly, no quantitative comparison with existing diagnostic standards (high-sensitivity troponin or electrocardiography) is provided, as such validation studies have not yet been conducted.

Conclusion:  The panel of ECE-1, AMPK, and ox-LDL shows theoretical diagnostic potential for T2DM-AMI based on existing mechanistic studies. However, because this is a narrative review without original patient data, clinical cohorts, or laboratory measurements, clinical validation in prospective studies is required before any diagnostic application can be recommended. However, without established diagnostic criteria, quantitative metrics (sensitivity, specificity, AUC-ROC, cutoff values), or direct quantitative comparison with current standards (hs-troponin, ECG), the term "diagnosis" remains aspirational. Clinical validation studies reporting these quantitative measures are urgently needed.