Juan de la Puente-Aldea

Mr. Juan de la Puente-Aldea

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Research Focus & Metrics

Academic Career Length

3Years (2024-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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LGLucía González-Gutiérrez
Lucía González-Gutiérrez
OGOmar Motiño Garcia-Miguel
Omar Motiño Garcia-Miguel
DPDaniel Barriuso Palacios
Daniel Barriuso Palacios
JPJuan de la Puente-Aldea
Juan de la Puente-Aldea
LALucia Alvarez-Frutos
Lucia Alvarez-Frutos
LSLaura SENOVILLA
Laura SENOVILLA
Colorectal cancer (CRC) affects approximately 2 million people worldwide. Obesity is the major risk factor for CRC. In addition, obesity contributes to a chronic inflammatory stage that enhances tumor progression through the secretion of proinflammatory cytokines. In addition to an increased inflammatory response, obesity-associated cancer presents accrued molecular factors related to cancer characteristics, such as genome instability, sustained cell proliferation, telomere dysfunctions, angiogenesis, and microbial alteration, among others. Despite the evidence accumulated over the last few years, the treatments for obesity-associated CRC do not differ from the CRC treatments in normal-weight individuals. In this review, we summarize the current knowledge on obesity-associated cancer, including its epidemiology, risk factors, molecular factors, and current treatments. Finally, we enumerate possible new therapeutic targets that may improve the conditions of obese CRC patients. Obesity is key for the development of CRC, and treatments resulting in the reversal of obesity should be considered as a strategy for improving antineoplastic CRC therapies.

Verified
Journal Article
Open access
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JPJuan de la Puente-Aldea
Juan de la Puente-Aldea
OLOscar López Llanos
Oscar López Llanos
DNDaniel Horrillo Novero
Daniel Horrillo Novero
HMHortensia Marcos-Sanchez
Hortensia Marcos-Sanchez
SSSandra Sanz-Ballesteros
Sandra Sanz-Ballesteros
Roberto Palacios-RamirezRoberto Palacios-Ramirez
Roberto Palacios-Ramirez
The classical function of the mineralocorticoid receptor (MR) is to maintain electrolytic homeostasis and control extracellular volume and blood pressure. The MR is expressed in the central nervous system (CNS) and is involved in the regulation of the hypothalamic–pituitary–adrenal (HPA) axis as well as sleep physiology, playing a role in the non-rapid eye movement (NREM) phase of sleep. Some patients with psychiatric disorders have very poor sleep quality, and a relationship between MR dysregulation and this disorder has been found in them. In addition, the MR is involved in the regulation of the renal peripheral clock. One of the most common comorbidities observed in patients with chronic kidney disease (CKD) is poor sleep quality. Patients with CKD experience sleep disturbances, including reduced sleep duration, sleep fragmentation, and insomnia. To date, no studies have specifically investigated the relationship between MR activation and CKD-associated sleep disturbances. However, in this review, we analyzed the environment that occurs in CKD and proposed two MR-related mechanisms that may be responsible for these sleep disturbances: the circadian clock disruption and the high levels of MR agonist observed in CKD.

23 October 2025 in Clínica
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Journal Article
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ÁLÁngel Ugarte López
Ángel Ugarte López
JPJuan de la Puente-Aldea
Juan de la Puente-Aldea
DBDaniel Barriuso
Daniel Barriuso
LSLaura Senovilla
Laura Senovilla
Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor of the central nervous system. It exhibits high genetic and phenotypic heterogeneity, which complicates early diagnosis and limits therapeutic efficacy. Its incidence is approximately 3-4 cases per 100,000 inhabitants per year, with a higher prevalence in older adults. This type of tumor is associated with high mortality due to its rapid progression, tumor resistance, and the blood-brain barrier, which restricts drug access. This paper highlights the low efficacy of conventional therapeutic strategies, such as surgical resection, radiotherapy, and chemotherapy with temozolomide, and reviews therapies currently under investigation, including immunotherapy, personalized vaccines, viral vectors, CAR-T cells, and nanotechnology. The role of molecular biomarkers in prognosis and the selection of individualized therapies is also considered. The information comes from recent preclinical studies and clinical trials, providing a comprehensive overview of current knowledge and innovations in development to improve the treatment of GBM.