PTEN gene & TNF-alpha in acute myocardial infarction

Abstract

Background PTEN gene triggers cells to undergo apoptosis and promotes myocardial dysfunction. Several TNF family cytokines are elevated during acute myocardial infarction (AMI). Their role in predicting subsequent prognosis in these setting remains poorly understood. We assessed serum levels of PTEN gene activity & TNF-α in acute ST elevation myocardial infarction and determined the impact of their levels on both left ventricular function and the clinical outcome in these patients. Methods and results Seventy patients with AMI and seventy persons as control group were subjected to: ECG, echocardiography, serum TNF-α and PTEN gene assessment. Patients were classified into: Group I (n = 32): All had left ventricular systolic failure. Group II (n = 38): without left ventricular systolic failure. Group I had a statistically significant higher serum levels of both TNF-α & PTEN gene activity as compared to group II. EF% at presentation was weakly correlated with serum levels of both markers in both groups. However at follow up, EF% in group I showed a significant negative correlations with both serum levels of TNF-α and PTEN gene activity (r = 0.77 & r = 0.67, respectively). During one year follow, 5 patients died of cardiovascular causes and 6 patients had recurrent hospitalization with heart failure. These patients had statistically significant increased serum levels of TNF-α & PTEN gene activity levels as compared by other patients. Conclusions Patients with acute myocardial infarction had statistically significant increased serum levels of PTEN & TNF-α gene activity. Both markers predict worsening of left ventricular systolic functions, development of heart failure and death.

PTEN inhibitor improves vascular remodeling and cardiac function after myocardial infarction through PI3k/Akt/VEGF signaling pathway

“…As a tumor suppressor gene, PTEN is capable to inhibit the progressions of numerous tumors, from benign to the most malignant forms, in which angiogenesis was participated, namely angiogenic switch. Increasing evidence demonstrated that PTEN participated in the progression of myocardial infarction (Mahmoud et al 2019;Wu et al 2019), and patients with acute MI had increased levels of PTEN in the serum, which suggested that PTEN might be used as predict marker for MI. Moreover, varieties of candidates improved MI by regulating PTEN/PI3K/Akt pathway, such as miR-320 (Hu et al 2018), miR-26a (Zhang and Cui 2018), miR-144-3p (Yuan et al 2019) and Astragaloside IV (Cheng et al 2019).…”

Polimorfismo de genes de citocinas: ¿factores de riesgo cardiovascular en la población venezolana?

“…Ambos genotipos estarían asociados con producciones moderadas de estas citocinas, confiriendo protección frente al desarrollo de IAM. Diferentes estudios han descrito que los pacientes con SCA presentan concentraciones incrementadas de IL-6 17-21 y TNF [22][23][24][25][26][27] . La producción incrementada de IL-6 puede estar promoviendo la aterogénesis, contribuyendo al riesgo de IAM, o puede ser el resultado de la aterosclerosis, asociada con fuertes reacciones inflamatorias 28 .…”

Alterações Precoces nas Interleucinas Circulantes e no Risco Inflamatório Residual após Infarto Agudo do Miocárdio

“…Algumas citocinas inflamatórias capazes de ativar a via inflamatória mediada pela IL-6, como o fator de necrose tumoral-alfa (TNF-α) ou o IL-1R, não foram medidas e podem ter relevância nas respostas teciduais e na remodelação ventricular do paciente. 36 , 37 Na verdade, o IAM per se pode estar relacionado a um aumento na IL-6 como resposta a uma lesão. No entanto, os títulos de IL-6 permaneceram elevados enquanto outras citocinas alteraram seus níveis séricos após 30 dias do IAMCSST.…”

“…Some inflammatory cytokines capable of activating the inflammatory pathway mediated by IL-6, such as tumor necrosis factor-alpha (TNF-α) or IL-1R, were not measured and may have relevance in host tissue responses and ventricular remodeling. 36 , 37 In fact, MI per se could be related to an increase in IL-6 as a response to injury. However, IL-6 titers remained elevated while other cytokines changed their serum levels after 30 days of STEMI.…”