BACKGROUND: Acute myocardial infarction (AMI) is a main contributor of sudden cardiac death worldwide. The discovery of new biomarkers that can improve AMI risk prediction meets a major clinical need for the identification of high-risk patients and the tailoring of medical treatment. Previously, we reported that autophagy a highly conserved catabolic mechanism for intracellular degradation of cellular components is involved in atherosclerotic plaque phenotype and cardiac pathological remodeling. The crucial role of autophagy in the normal and diseased heart has been well described, and its activation functions as a pro-survival process in response to myocardial ischemia. However, autophagy is dysregulated in ischemia/reperfusion injury, thus promoting necrotic or apoptotic cardiac cell death. Very few studies have focused on the plasma levels of autophagy markers in cardiovascular disease patients, even though they could be companion biomarkers of AMI injury. The aims of the present study were to evaluate (1) whether variations in plasma levels of two key autophagy regulators autophagy-related gene 5 (ATG5) and Beclin 1 (the mammalian yeast ortholog Atg6/Vps30) are associated with AMI and (2) their potential for predicting AMI risk.
METHODS: The case-control study population included AMI patients (n = 100) and control subjects (n = 99) at high cardiovascular risk but without known coronary disease. Plasma levels of ATG5 and Beclin 1 were measured in the whole population study by enzyme-linked immunosorbent assay.
RESULTS: Multivariate analyses adjusted on common cardiovascular factors and medical treatments, and receiver operating characteristic curves demonstrated that ATG5 and Beclin 1 levels were inversely associated with AMI and provided original biomarkers for AMI risk prediction.
CONCLUSIONS: Plasma levels of autophagy regulators ATG5 and Beclin 1 represent relevant candidate biomarkers associated with AMI.

Implantation is a key point in pathological processes associated with infertility, especially in endometriosis. In this complex process, there is limited evidence to demonstrate the role of receptivity and autophagy. The present study aimed to evaluate LC3A/B, P62/SQSTM1, Beclin 1, and integrin expressions and receptivity and autophagy processes in endometriosis in pregnant rats with healthy endometriosis on day 6 of the process. Pregnancy was observed in all rats in the control group (8/8), while the pregnancy was 4/8 in the endometriosis group, and 6/8 in the endometriosis + ALA group. LC3A/B and P62/SQSTM1 expression increased significantly in the endometriosis + ALA group, compared with endometriosis groups (p < .05). The effect of ALA on autophagy and receptivity in endometriosis was shown for the first time. Antioxidant and anti-inflammatory treatments in endometriosis should be investigated as new treatment modalities for implantation problems. PRACTICAL APPLICATIONS: Endometriosis, the etiology of which remains unknown, is an important cause of infertility. Implantation is the key point in pathological processes associated with infertility. In this complex process, there is limited evidence to demonstrate the role of receptivity and autophagy. The present study aimed to evaluate LC3A/B, P62/SQSTM1, Beclin 1, and integrin expressions and receptivity and autophagy processes in endometriosis in pregnant rats with healthy endometriosis on day 6 of the process. Oral alpha-lipoic acid was administered to one group and the effect of this powerful antioxidant on the process was evaluated.

BACKGROUND: Cigarette smoking causes a variety of adverse human health effects, including lung cancer. The molecular events associated with smoke-induced carcinogenesis are thought to be related in part to autophagy. Beclin 1 is an important autophagy-related protein involved in cell death and cell survival.
OBJECTIVE: The purpose of this investigation was to determine the beclin 1 protein and its association with cigarette smoke and the mutation of epidermal growth factor receptor (EGFR) in non-small cell lung cancer (NSCLC).
METHODS: Our study included 108 cases of non-small cell lung cancer who were admitted in our hospital. The beclin 1 protein was detected by immunohistochemistry and EGFR mutation by direct sequencing.
RESULTS: Beclin 1 expression could be detected in 15 (13.9%) of 108 specimens. These studies investigated that beclin 1 expression was associated with heavy smoking, the gender and the histological type of NSCLC (P = 0.023, 0.035 and 0.039). No association of beclin 1 with EGFR mutation was found (P > 0.05).
CONCLUSIONS: The results from these experiments indicate that heavy smoking may induce the beclin 1 protein in NSCLC.

The aim of the present study was to evaluate the expressions of beclin 1 and bcl-2 in prostate cancer (PC) and high grade prostatic intraepithelial neoplasia (HGPIN), and to investigate their relationship with clinicopathological parameters. The study included 30 benign prostatic hyperplasia (BPH), 40 HGPIN and 106 primary PC cases. The expressions of beclin 1 and bcl-2 were assessed semiquantitatively based on both the percentage and intensity of positive staining cells. Beclin 1 was positive in 27 (90%) BPH, 37 (92.5%) HGPIN, and 90 (84.9%) PC cases (p>0.05). Bcl-2 immunostaining was detected in 99 (93.4%) PC, 37 (92.5%) HGPIN, and 9 (30%) BPH cases (p<0.0001). Regarding expression scores, beclin 1 was significantly lower in PC cases than in the HGPIN and BPH groups (p<0.0001), and it was also negatively correlated with Gleason score (p=0.004, r=-0.274). Bcl-2 expression score was significantly higher in PC than in the other groups (p<0.0001), and also positively correlated with Gleason score (p<0.0001, r=0.425). Furthermore, a negative correlation was found between bcl-2 and beclin 1 expression scores in PC cases (p=0.006, r=-0.265). Our results suggest an association between bcl-2 and beclin 1 expressions in malignant transformation of prostate tissue and also in regulating PC cell differentiation, progression and the aggressiveness of PC.