Person:
Candel González, Francisco Javier

Profile Picture
First Name
Francisco Javier
Last Name
Candel González
URI
https://hdl.handle.net/20.500.14352/79145
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Medicina
Area
Microbiología
Identifiers
UCM identifierScopus Author IDDialnet ID

Filters

2022 - 20242
Reset filters

Settings

Author: Anguita Mandly, Eduardo Luis ×

Search Results

Now showing 1 - 2 of 2
  • Thumbnail Image
    Item
    Biomarkers of stable and decompensated phases of heart failure with preserved ejection fraction
    (International journal of cardiology, 2022) Anguita Mandly, Eduardo Luis; Chaparro, Alberto; Candel González, Francisco Javier; Ramos Acosta, Carlos; Torrejón, María José; Llopis García, Guillermo; Suárez Cadenas, María del Mar; Matesanz, Mayra; González Del Castillo, Juan María; Martín Sánchez, Francisco Javier; Anguita, Eduardo
    Background Heart failure with preserved ejection fraction (HFpEF) is a disorder related to patient comorbidities and aging. Whether mitochondrial dysfunction is present during HFpEF decompensation versus the stable phase is largely unknown. The aim of the present study was to identify mitochondrial and cell metabolism blood biomarkers in older patients with acute and stable HFpEF. Methods Peripheral blood biomarkers were investigated in a group of eight to 12 patients aged 80–96 years and diagnosed with HFpEF first when they were in decompensated phase and then at least three months later in stable phase. Their data were compared to two control groups with an equal number of participants and sex proportions. One group was age matched and the other included individuals aged between 22 and 44 years. Results Decompensated patients experienced an increased mitochondrial superoxide production and mitochondrial mass, lower mitochondrial DNA copy number and LDHB expression, and higher lactate level compared to the stable stage. The stable phase was characterized by a sharp reduction in formate level. Multivariate analysis indicated that formate, lactate, and histidine can distinguish both of the HFpEF phases. Many of these parameters, including LDHB, lactate, formate, and mitochondrial mass, followed an age-related pattern, with acute HFpEF at its apex or nadir, suggesting that it represents an exacerbation of an aging-related process. Conclusions We identified distinct blood biomarkers of chronic and decompensated HFpEF phases. The data underlined the relationship between HFpEF and aging. These findings could be used to monitor patients and might be therapeutically targeted.
  • Thumbnail Image
    Item
    Tigecycline Opposes Bortezomib Effect on Myeloma Cells Decreasing Mitochondrial Reactive Oxygen Species Production
    (International journal of molecular sciences, 2024) Ramos Acosta, Carlos; Huerta Pantoja, Laura; Salazar Hidalgo, Milton Eduardo; Mayol, Elsa; Jiménez Vega, Selene; García Peña, Pablo; Jordi Cruz, Jenifeer; Baquero, Cristina; Porras Gallo, María Almudena; Íñigo Rodríguez, Belén; Benavente Cuesta, Celina; Candel González, Francisco Javier; Anguita Mandly, Eduardo Luis
    Multiple myeloma is an incurable plasma cell malignancy. Most patients end up relapsing and developing resistance to antineoplastic drugs, like bortezomib. Antibiotic tigecycline has activity against myeloma. This study analyzed tigecycline and bortezomib combination on cell lines and plasma cells from myeloma patients. Apoptosis, autophagic vesicles, mitochondrial mass, mitochondrial superoxide, cell cycle, and hydrogen peroxide were studied by flow cytometry. In addition, mitochondrial antioxidants and electron transport chain complexes were quantified by reverse transcription real-time PCR (RT-qPCR) or western blot. Cell metabolism and mitochondrial activity were characterized by Seahorse and RT-qPCR. We found that the addition of tigecycline to bortezomib reduces apoptosis in proportion to tigecycline concentration. Supporting this, the combination of both drugs counteracts bortezomib in vitro individual effects on the cell cycle, reduces autophagy and mitophagy markers, and reverts bortezomib-induced increase in mitochondrial superoxide. Changes in mitochondrial homeostasis and MYC upregulation may account for some of these findings. These data not only advise to avoid considering tigecycline and bortezomib combination for treating myeloma, but caution on the potential adverse impact of treating infections with this antibiotic in myeloma patients under bortezomib treatment.