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Rivera Caravaca, José Miguel

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Rivera Caravaca, José Miguel
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Universidad de Murcia. Departamento de Enfermería
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    Analysis of key proinflammatory mechanisms in cardiovascular pathology through stimulation with lipopolysaccharide and urban particulate matter in mouse atrial cardiomyocytes
    (Elsevier, 2025-02-09) Mandaglio-Collados, Darío; Ruiz Alcaraz, Antonio José; Rivera Caravaca, José Miguel; Ramos-Bratos, María Pilar; Marín Ortuño, Francisco; López Gálvez, Raquel; Bioquímica y Biología Molecular B e Inmunología; Facultad de Biología
    Air pollution has emerged as one of the leading causes of mortality, aggravating cardiovascular diseases. Urban-particulate matter (PM) can accumulate in the cardiovascular system and through inflammation, trigger systemic damage. One of the key mechanisms of this process could be related to the activation of the inflammasome through the pre-existence of a low-grade endotoxemia and PM presence in the cells. Herein, we studied the deleterious effects of urban-PM and Lipopolysaccharide (LPS) exposure in a HL-1 mouse cardiomyocyte cell line. Urban-PM induced biological changes, including mRNA expression of pro-inflammatory genes, intracellular reactive oxygen species (ROS) generation and overexpression of inflammasome-related and structural proteins. The results revealed that urban-PM with different ultrastructure, as determined by transmission electron microscopy (TEM), is embedded inside the cardiomyocytes, leading to the recognition and activation of the inflammatory process. The increase of ROS levels and mRNA levels of pro-inflammatory genes were similarly observed in a dose-dependent manner. In addition, components and proteins of the inflammasome such as associated speck-like protein containing a CARD (ASC), caspase-1 and IL-1β were differentially overexpressed in treated HL-1 cells, as well as structural proteins like Connexin 43 (Cx43). These results provide new insights into the mechanisms that mediate innate pro-inflammatory activation in cardiomyocytes in response to air suspension pollutants.
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    Endothelial activation, cell-cell interactions, and inflammatory pathways in postoperative atrial fibrillation following cardiac surgery
    (Elsevier, 2024-11-26) López-Gálvez, Raquel; Rivera Caravaca, José Miguel; Mandaglio-Collados, Darío; Ruiz Alcaraz, Antonio José; Lahoz-Tornos, Álvaro; Hernández Romero, Diana; Orenes-Piñero, Esteban; Ramos-Bratos, María Pilar; Martínez Cáceres, Carlos Manuel; Carpes, Marina; Arribas Leal, José María; Cánovas López, Sergio Juan; Lip, Gregory Y.H.; Marín Ortuño, Francisco; Bioquímica y Biología Molecular B e Inmunología; Facultad de Biología
    Background. Postoperative atrial fibrillation (POAF) is common after cardiac surgery and related to endothelial activation and systemic inflammation. Herein, we investigate the pathophysiological mechanisms of AF through endothelial activation and cell-cell interactions related to the development of POAF. Methods. Patients without previous AF undergoing cardiac surgery were studied. Permanent AF patients were included as positive controls. Interleukin (IL)-6, Von Willebrand factor (vWF), N-terminal pro-brain natriuretic peptide (NT-proBNP), and high sensitivity troponin T (hsTnT) were evaluated by electrochemiluminescence. Vascular cell adhesion molecule-1 (VCAM-1) and human Growth Differentiation Factor 15 (GDF-15) were assessed by ELISA. Connexins (Cxs) 40 and 43 were measured by tissue immunolabelling, and apoptosis by TUNEL assay. Results. We included 117 patients (median age 67: 27.8% female): 17 with permanent AF; 27 with POAF, and 73 with non-AF. Patients with permanent AF and POAF had higher levels of NT-proBNP, hs-TnT, apoptotic nuclei, and decreased Cx43 expression, compared to non-AF patients (all p-value <0.05). VCAM-1 and GDF-15 were significantly higher in permanent AF vs. non-AF (p = 0.013 and p = 0.035). Conclusions. Greater endothelial activation and inflammation in AF patients compared to those without AF were found. The proinflammatory state in AF patients, in addition to the lower expression of Cx43, seems to be associated with atrial remodeling processes occurring in AF.
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    Impact of particulate matter on the incidence of atrial fibrillation and the risk of adverse clinical outcomes: a review
    (Elsevier, 2023-04-04) Mandaglio-Collados, Darío; López-Gálvez, Raquel; Ruiz Alcaraz, Antonio José; López-García, Cecilia; Roldán Schilling, Vanessa; Lip, Gregory Y.H.; Marín Ortuño, Francisco; Rivera Caravaca, José Miguel; Bioquímica y Biología Molecular B e Inmunología; Facultad de Biología
    Background. Atrial fibrillation (AF) is common and increases the risk of stroke and mortality. Previous studies have suggested that air pollution is an important risk factor for new-onset AF. Herein, we review the evidence regarding: 1) the association between exposure to particulate matter (PM) and new-onset AF, and 2) the risk of worse clinical outcomes in patients with pre-existent AF and their relation to PM exposure. Methods. A selection of studies between 2000 and 2023 linking PM exposure and AF was performed through searches in PubMed, Scopus, Web of Science, and Google Scholar. Results. 17 studies from different geographical areas demonstrated that exposure to PM was associated with an increased risk of new-onset AF, although the results were heterogeneous regarding the temporal pattern (short- or long-term) ultimately related to AF. Most of the studies concluded that the risk of new-onset AF increased between 2 %–18 % per 10 μg/m3 increment in PM2.5 or PM10 concentrations, whereas the incidence (percentage of change of incidence) increased between 0.29 %–2.95 % per 10 μg/m3 increment in PM2.5 or PM10. Evidence about the association between PM and adverse events in patients with pre-existent AF was scarce but 4 studies showed a higher risk of mortality and stroke (between 8 %–64 % in terms of hazard ratio) in patients with pre-existent AF when PM exposure was higher. Conclusions. Exposure to PM (both PM2.5 and PM10) is a risk factor for AF, and a risk factor for mortality and stroke in patients who already suffer from AF. Since the relationship between PM and AF is independent of the region of the world, PM should be considered as a global risk factor for both AF and worse clinical outcomes in AF patients. Specific measures to prevent air pollution exposure need to be adopted.
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