Dysregulation of the MEG3–ATF4 Axis in ST-Segment Elevation Myocardial Infarction: A Proof-of-Concept Study

Background/Objectives: Cardiovascular disease is the leading cause of morbidity and mortality worldwide, of which the myocardial Infarction is the most prevalent. However, the underlying pathophysiological mechanisms remain incompletely understood, but are tightly regulated by several cellular mechanisms, including long-non-coding. This study aimed to determine if MEG3 and ATF4 are involved in this pathology. Methods: A cross-section study was conducted at the Instituto Nacional de Cardiología Ignacio Chávez, patients with first time diagnosis STEMI and hemodynamic stability were categorized into with and without major adverse cardiovascular events, the most important clinical and biochemical parameters were collected, which were analyzed and subsequently correlated with MEG3 and ATF4. Results: Forty-two patients with a median age of 54 years (86% men) were included and classified with and without MACE. The expression of MEG3 in MACE group and No MACE (0.8974, 0.4186–1.4131 vs. 1.2259, 0.5516–2.3964; p = 0.0342), and ATF4 in MACE group and No MACE (2.8950, 0.7559–4.3287 vs. 2.3498, 1.0821–3.6903; p = 0.0396), ROC curve MEG3 showed an AUC of 0.6490 (0.4760 to 0.8221; p = 0.0924), in contrast ATF4 demonstrated an AUC of 0.7127 (0.5862 to 0.8393; p = 0.0107). Finally, correlation analyses revealed MEG3 was associated with CK-MB (r = 0.3978, 0.0630 to 0.6520; p = 0.0219), and ATF4 was correlated cTnT (r = 0.3328, 0.0284 to 0.5810; p = 0.0335) and with LVEF (r = –0.4283, –0.6503 to –0.1390; p = 0.0052). Conclusions: The dysregulation of MEG3 and transcription factor ATF4 are involved in pathophysiological mechanisms.