Dr. Óscar López-Franco is a Senior Research in University of Veracruz-México. Graduate in Biochemistry by Complutense University and Doctorate with Honours by Autonoma University (Madrid-Spain, 1998 and 2004, respectively). More than 20 years of research experience. During this time (from 1999 to 2013) he has worked in three laboratories: Renal and Vascular Research Group (Jimenez Diaz Foundation, Madrid, Spain); Cardiovascular Research Group and Biomedical Research Group, both in University of Glasgow, UK. Since 2014, he has led the group “Translational Medicine” in the Health Science Institute of the University of Veracruz. His research activities focus on the molecular mechanisms of immune renal, diabetes and atherosclerosis diseases, with special interest in Fc receptors, SOCS proteins, gene therapy and microRNAs. Working as part of a multidisciplinary groups composed of both scientist and clinicians has been invaluable in developing research projects.
EDUCATION
Graduate in Biochemistry by Complutense University (Madrid-Spain, 1998)
Doctorate with Honours by Autonoma University (Madrid-Spain, 2004)
RESEARCH, TEACHING, or OTHER INTERESTS
Molecular Medicine, Drug Discovery, Biochemistry, Genetics and Molecular Biology
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Scopus Publications
Scopus Publications
Opposing functions of miR-155-5p and Socs1 drive vascular inflammation in diabetes-accelerated atherosclerosis María Kavanagh, Isabel Herrero del Real, Ignacio Prieto, Raquel Alvarez-Moreno, Jesus Egido, Oscar Lopez-Franco, Iolanda Lázaro, Carmen Gomez-Guerrero Cardiovascular Diabetology, 2026 BACKGROUND: Diabetes accelerates atherosclerosis by driving persistent vascular inflammation. MicroRNA-155 (miR-155) is a post-transcriptional regulator of inflammatory genes, while suppressor of cytokine signaling 1 (Socs1) limits Janus kinase (JAK)/signal transducer and activator of transcription (STAT)-mediated cytokine responses. We explored how the imbalance between miR-155-5p and Socs1 contributes to atherosclerotic plaque progression in diabetes. METHODS: Apolipoprotein E knockout (ApoE-/-) mice were studied in two settings: age-dependent atherosclerosis progression under non-diabetic conditions, and streptozotocin-induced diabetes to model accelerated atherosclerosis. Diabetic mice received a miR-155-5p inhibitor, a Socs1-expressing adenovirus, or respective controls. Lesion size, composition, and gene expression were analyzed. Cultured vascular smooth muscle cells (VSMCs) and macrophages were transfected with miR-155-5p mimic/inhibitor and Socs1 siRNA/plasmid to assess inflammatory responses, phenotypes, and efferocytosis under diabetic-like conditions. RESULTS: During atherosclerosis progression, vascular miR-155-5p inversely correlated with Socs1 and positively with lesion size, while Socs1 correlated negatively with plaque burden. In diabetic mice, miR-155-5p inhibition reduced lesion area, lipid/collagen and macrophage/VSMC ratios, pro-inflammatory cytokines, M1 macrophages and synthetic VSMC markers, while increasing Socs1, M2 and contractile VSMC genes. Socs1 gene transfer reproduced these effects by reducing miR-155-5p and Stat1 expression, and lesion size. In vitro, miR-155-5p mimic suppressed Socs1, activated STAT1 and inflammatory phenotypes in macrophages and VSMCs, whereas miR-155-5p inhibition had opposite effects. Socs1 silencing amplified inflammation, and its overexpression counteracted miR-155-5p actions. Moreover, miR-155-5p inhibition reduced soluble Mer receptor tyrosine kinase (MerTK) in plaques and macrophages, indicating improved efferocytosis, whereas the mimic promoted macrophage MerTK shedding and impaired apoptotic cell clearance. CONCLUSION: Reciprocal regulation between miR-155-5p and Socs1 influences vascular inflammation, phenotypic changes, and defective efferocytosis in a diabetic context. Targeting this axis may restore resolution mechanisms and enhance plaque stability in diabetes-associated vascular disease.
Ovarian influence on circadian and infradian modulation of nicotine-seeking in female mice Zenaida Rosas‐Ovando, Gisela Aguirre, Tania Molina‐Jiménez, Mónica Flores‐Muñoz, Óscar López‐Franco, Rossana C. Zepeda, Aleph A. Corona‐Morales, Armando Jesús Martínez, Roberto C. Salgado‐Delgado, Claudia Juárez‐Portilla Journal of Neuroendocrinology, 2026 Sex differences in tobacco intake are closely associated with hormonal fluctuations during the menstrual cycle in women. Elevated estrogen levels have been associated with increased stress, which may lead to a higher likelihood of seeking psychoactive substances. Additionally, tobacco use has been associated with negative effects on reproductive health. Preclinical studies suggested that the estrous cycle significantly influences addictive behaviors, emphasizing the role of ovarian hormones. Furthermore, psychoactive substances entrain circadian rhythms, with animals showing increased locomotor activity 1–2 h before drug administration time, known as anticipatory activity, reflecting seeking behavior. This study aims to evaluate the impact of ovarian hormones on nicotine‐anticipatory behavior. A circadian model of forced administration of nicotine via nebulization was implemented in intact and ovariectomized female mice, exposing them to nicotine at a fixed time (ZT4) for 20 min daily over 14 days. The effects of nicotine intake on ovarian follicle morphology and maturation were also assessed. Daily nicotine exposure successfully entrained a clear anticipatory behavior in intact mice. Notably, this anticipatory activity was completely abolished in ovariectomized females, indicating a critical dependence on ovarian factors. Furthermore, nicotine exposure disrupted the estrous cycle and induced significant ovarian follicular damage in intact females. Our findings suggest that the hormonal state is a primary modulator of nicotine‐anticipatory behavior. Moreover, the observed nicotine‐induced ovarian damage highlights a significant risk to female reproductive health, suggesting a bidirectional relationship between nicotine use and the hypothalamic–pituitary–gonadal axis.
Ovarian Hormones and Addictive Behaviour Vulnerability: Insights From Preclinical Studies Leonardo Vázquez‐Morales, Gisela Aguirre, Tania Molina‐Jiménez, Rossana C. Zepeda, Óscar López‐Franco, Mónica Flores‐Muñoz, Claudia Juárez‐Portilla Addiction Biology, 2025 Substance use disorder constitutes a global health challenge. Preclinical investigations into addiction heavily rely on animal models to explore the underlying biological mechanisms of addictive disorders, with a particular emphasis on understanding the etiological factors influencing drug intake. Exploring sex differences across various phases of addiction has revealed a heightened vulnerability in females. This study systematically reviews the impact of ovarian hormones on the consumption of psychoactive substances in rodents, adhering to the PRISMA 2009 protocol. Our findings underscore the significant role of ovarian hormones, particularly oestrogen, in augmenting drug consumption among female rodents. Notably, with heroin, it was observed that progesterone, rather than oestrogen, facilitated increased consumption in female rodents. The susceptibility to addiction influenced by oestrogen is accentuated across distinct phases, and the molecular mechanisms form a complex interplay that significantly influences addictive behaviours. By bringing together these findings, we aim to establish a strong foundation for future studies. This work may guide clinical investigations in developing more effective prevention or treatment strategies that address the unique vulnerabilities of females to substance use disorders.
Counter-regulatory RAS peptides: new therapy targets for inflammation and fibrotic diseases? Diana V. Ávila-Martínez, Wendy K. Mixtega-Ruiz, José M. Hurtado-Capetillo, Oscar Lopez-Franco, Mónica Flores-Muñoz Frontiers in Pharmacology, 2024 The renin-angiotensin system (RAS) is an important cascade of enzymes and peptides that regulates blood pressure, volume, and electrolytes. Within this complex system of reactions, its counter-regulatory axis has attracted attention, which has been associated with the pathophysiology of inflammatory and fibrotic diseases. This review article analyzes the impact of different components of the counter-regulatory axis of the RAS on different pathologies. Of these peptides, Angiotensin-(1–7), angiotensin-(1–9) and alamandine have been evaluated in a wide variety of in vitro and in vivo studies, where not only they counteract the actions of the classical axis, but also exhibit independent anti-inflammatory and fibrotic actions when binding to specific receptors, mainly in heart, kidney, and lung. Other functional peptides are also addressed, which despite no reports associated with inflammation and fibrosis to date were found, they could represent a potential target of study. Furthermore, the association of agonists of the counter-regulatory axis is analyzed, highlighting their contribution to the modulation of the inflammatory response counteracting the development of fibrotic events. This article shows an overview of the importance of the RAS in the resolution of inflammatory and fibrotic diseases, offering an understanding of the individual components as potential treatments.
A mutual regulatory loop between miR-155 and SOCS1 influences renal inflammation and diabetic kidney disease Ignacio Prieto, María Kavanagh, Luna Jimenez-Castilla, Marisa Pardines, Iolanda Lazaro, Isabel Herrero del Real, Monica Flores-Muñoz, Jesus Egido, Oscar Lopez-Franco, Carmen Gomez-Guerrero Molecular Therapy Nucleic Acids, 2023 , SOCS1 gene delivery decreased miR-155-5p and kidney injury in diabetic mice. Moreover, therapeutic inhibition of miR-155-5p suppressed STAT1/3 activation and alleviated albuminuria, mesangial damage, and renal expression of inflammatory and fibrotic genes. In conclusion, modulation of the miR-155/SOCS1 axis protects kidneys against diabetic damage, thus highlighting its potential as therapeutic target for DKD.
Beneficial effects of an algal oil rich in ω-3 polyunsaturated fatty acids on locomotor function and D2 dopamine receptor in haloperidol-induced parkinsonism Alejandra Barroso-Hernández, Abril Ramírez-Higuera, Carolina Peña-Montes, Sergio Alberto Cortés-Ramírez, Mauricio Rodríguez-Dorantes, Óscar López-Franco, Rosa María Oliart-Ros Nutritional Neuroscience, 2022 Introduction: Parkinson's disease (PD) is a chronic neurological disorder whose pathogenesis involves the loss of dopaminergic neurons and dopamine terminals, formation of Lewy bodies, and microgliosis. Its treatment includes dopamine-based drugs with limited results and adverse effects. Additionally, some neuroleptic drugs used for mental disorders produce side effects referred to as parkinsonism. Dietary interventions with ω-3 polyunsaturated fatty acids (ω-3 PUFA) have attracted attention since they play a key role in most of the processes associated with PD etiology. Objective: The purpose of our work was to investigate the effects of an ω-3 PUFA rich algal oil on locomotive alterations induced by haloperidol and D2 receptor protein and gene expression in Wistar rats. Methodology: Pre- and co-supplementation of algal oil (300 mg of ω-3 FA/kg/day for six weeks) and haloperidol (1.5 mg/kg/day for two weeks) were evaluated. Results: Haloperidol provoked locomotive alterations in the Open Field Test and a 43% diminution in D2 receptor in brain membranes; in pre-supplemented rats a 93% increase in D2 receptor protein expression and a partial maintenance of locomotory performance were observed, while in co-supplemented rats D2 receptor protein expression was maintained as in control rats, although locomotive behavior was found diminished as in haloperidol rats. Conclusions: These results confirm the beneficial effects of ω-3 PUFA over locomotory alterations and as neuroprotective and neurorestorative compounds and demonstrates a stimulatory action on D2 receptor presence, as a mechanism by which these fatty acids participate in brain health.
Cognitive Impairment After Resolution of Hepatic Encephalopathy: A Systematic Review and Meta-Analysis Óscar López-Franco, Jean-Pascal Morin, Albertina Cortés-Sol, Tania Molina-Jiménez, Diana I. Del Moral, Mónica Flores-Muñoz, Gabriel Roldán-Roldán, Claudia Juárez-Portilla, Rossana C. Zepeda Frontiers in Neuroscience, 2021 Hepatic encephalopathy (HE) is one of the most disabling metabolic diseases. It consists of a complication of liver disease through the action of neurotoxins, such as excessive production of ammonia from liver, resulting in impaired brain function. Its prevalence and incidence are not well known, although it has been established that up to 40% of cirrhotic patients may develop HE. Patients with HE episodes display a wide range of neurological disturbances, from subclinical alterations to coma. Recent evidence suggests that the resolution of hepatic encephalopathy does not fully restore cognitive functioning in cirrhotic patients. Therefore, the aim of this review was to evaluate the evidence supporting the presence of lingering cognitive deficits in patients with a history of HE compared to patients without HE history and how liver transplant affects such outcome in these patients. We performed two distinct meta-analysis of continuous outcomes. In both cases the results were pooled using random-effects models. Our results indicate that cirrhotic patients with a history of HE show clear cognitive deficits compared to control cirrhotic patients (Std. Mean Difference (in SDs) = −0.72 [CI 95%: −0.94, −0.50]) and that these differences are not fully restored after liver transplant (Std. Mean Difference (in SDs) = −0.48 [CI 95%: −0.77, −0.19]).
Fcγ receptor deficiency attenuates diabetic nephropathy Virginia Lopez-Parra, Beñat Mallavia, Oscar Lopez-Franco, Guadalupe Ortiz-Muñoz, Ainhoa Oguiza, Carlota Recio, Julia Blanco, Falk Nimmerjahn, Jesus Egido, Carmen Gomez-Guerrero Journal of the American Society of Nephrology, 2012
Suppressors of cytokine signaling abrogate diabetic nephropathy Guadalupe Ortiz-Muñoz, Virginia Lopez-Parra, Oscar Lopez-Franco, Paula Fernandez-Vizarra, Beñat Mallavia, Claudio Flores, Ana Sanz, Julia Blanco, Sergio Mezzano, Alberto Ortiz, Jesus Egido, Carmen Gomez-Guerrero Journal of the American Society of Nephrology, 2010
Heat shock proteins as potential therapeutic targets in atherosclerosis Julio Madrigal-Matute, Óscar López-Franco, Luis M. Blanco-Colio, Begoña Muñoz-García, Priscila Ramos-Mozo, Melany Van Oostrom, Olivier Meilhac, Jean-Baptiste Michel, Jesús Egido, José L. Martín Ventura Clinica E Investigacion En Arteriosclerosis, 2009
