Acute ST-elevation myocardial infarction (STEMI) leads to myocardial injury or necrosis, and M1 macrophages play an important role in the inflammatory response. Bone marrow mesenchymal stem/stromal cells (BM-MSCs) are capable of modulating macrophage plasticity, principally due to their immunoregulatory capacity. In the present study, we analyzed the capacity of MSCs to modulate macrophages derived from monocytes from patients with STEMI. We analyzed the circulating levels of cytokines associated with M1 and M2 macrophages in patients with STEMI, and the levels of cytokines associated with M1 macrophages were significantly higher in patients with STEMI than in controls. BM-MSCs facilitate the generation of M1 and M2 macrophages. M1 macrophages cocultured with MSCs did not have decreased M1 marker expression, but these macrophages had an increased expression of markers of the M2 macrophage phenotype (CD14, CD163 and CD206) and IL-10 and IL-1Ra signaling-induced regulatory T cells (Tregs). M2 macrophages from patients with STEMI had an increased expression of M2 phenotypic markers in coculture with BM-MSCs, as well as an increased secretion of anti-inflammatory cytokines and an increased generation of Tregs. The findings in this study indicate that BM-MSCs have the ability to modulate the M1 macrophage response, which could improve cardiac tissue damage in patients with STEMI.

Macrophages in atherosclerosis and myocardial infarction have diverse functions, such as foam cell formation and the induction of an inflammatory response that promotes ventricular dysfunction in the heart. Exosomes are small vesicles released by many different types of cells, such as macrophages, dendritic cells, platelets and other immunoregulatory cells, that facilitate communication with other cells, modulating the biological functions of recipient cells. Exosomes offer a novel therapeutic approach for the polarization of macrophages involved in cardiovascular diseases. In this review, we provide an overview of the biological role of macrophages in atherosclerosis and myocardial infarction and the effects of exosomes on these cells as therapeutic agents in the disease.

Occult HCV infection (OCI) is defined by the presence of HCV RNA in hepatocytes and/or peripheral blood mononuclear cells (PBMCs) without detectable HCV RNA or anti-HCV antibodies in plasma. OCI is underrecognized and may contribute to HCV transmission. This study estimated OCI prevalence and associated risk factors in adults from Mexico City. Methods: A retrospective cross-sectional study was conducted, analyzing 507 general population volunteers. Demographic data and potential risk factors were collected via questionnaire. Anti-HCV detection was performed using two techniques: immunochromatographic rapid test and chemiluminescent microparticle immunoassay (CMIA). Nested PCR was employed to detect HCV RNA in plasma and PBMCs. Positive samples were genotyped through sequencing and phylogenetic analysis of the Core/E1 region. Results: Of 507 participants, four were anti-HCV positive. HCV RNA was found in PBMCs of 27 individuals, while plasma samples tested negative, indicating a 5.3% OCI prevalence. OCI was significantly associated with blood donation (p = 0.015), drug use (p = 0.019), particularly cocaine (p = 0.001), and endoscopy (p = 0.043). Genotypes 1b, 1a, 2b, 3a, and 2j were detected in OCI cases. Conclusions: OCI prevalence in Mexico City’s general population is notable, with significant links to blood donation, cocaine use, and endoscopy. Enhanced diagnostic strategies are crucial to detect OCI and mitigate HCV transmission.

Background/Objectives: Aortic stenosis (AS) is the most prevalent valvular disease among older adults. Although obstructive sleep apnea (OSA) has been linked to adverse cardiovascular outcomes, its specific impact on patients with severe AS remains unclear. This study aimed to determine the prevalence of OSA and its influence on postoperative recovery following aortic valve replacement. Methods: A prospective case-control study was conducted at the Instituto Nacional de Cardiología Ignacio Chávez. Patients aged 40–80 years with echocardiographically confirmed severe AS were categorized into groups with and without OSA, based on respiratory polygraphy (Apnea–Hypopnea Index [AHI] threshold of >15 events per hour). Clinical, biochemical, echocardiographic, body composition, and hemodynamic parameters were assessed. Daytime sleepiness and sleep quality were evaluated using validated questionnaires. Inflammatory biomarkers were also analyzed. This study was approved by the institutional ethics committee. Results: Of the 30 patients included, 66.6% were diagnosed with OSA. Compared to non-OSA patients, those with OSA had a higher left ventricular mass index (160 vs. 108; p = 0.001), greater postoperative increases in central venous pressure [8 (8–10) vs. 8 (6–8); p = 0.037], and lower mixed venous oxygen saturation within the first 24 h (69.2 vs. 76; p = 0.027). OSA patients also had longer hospital stays (11 vs. 8 days; p = 0.014). Trends toward a heightened subclinical inflammatory state were noted in the OSA group. Conclusions: OSA is frequent and underdiagnosed in patients with severe AS and is associated with more complicated postoperative recovery. Systematic OSA screening is recommended for candidates undergoing aortic valve surgery.

This study aimed to evaluate whether serum from patients with primary antiphospholipid syndrome (APS) is associated with changes in the expression of long non-coding RNAs (lncRNAs) in endothelial cells. Human umbilical vein endothelial cells (HUVECs) were cultured with serum from 12 female patients with APS or 8 age-matched healthy female controls. The expression levels of HIF1A-AS1, OIP5-AS1, and GAS5 were quantified by RT-qPCR. Exposure of HUVECs to APS serum was associated with reduced expression of HIF1A-AS1 and OIP5-AS1 compared with cells stimulated with control serum. The median HIF1A-AS1 expression levels were 0.08 a.u. (interquartile range, 0.06–0.10) in APS-stimulated cells versus 0.14 a.u. (0.08–0.16) in controls (p = 0.044). Likewise, OIP5-AS1 levels were 0.09 a.u. (0.01–0.16) in APS-stimulated cells versus 2.24 a.u. (0.70–3.55) in controls (p = 0.018). In contrast, GAS5 expression did not differ significantly between groups (340 a.u. (310–3940 versus 358 a.u. (163–445); p = 0.290). In this proof-of-concept study, serum from APS patients was associated with selective downregulation of HIF1A-AS1 and OIP5-AS1 in endothelial cells. These findings support a potential link between circulating APS-related factors and endothelial lncRNA expression; however, no mechanistic or functional conclusions can be drawn.