David Cotán

ORCID: 0000-0001-9491-8899
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About
Contact & Profiles
Research Areas
  • Mitochondrial Function and Pathology
  • Fibromyalgia and Chronic Fatigue Syndrome Research
  • Coenzyme Q10 studies and effects
  • Cell death mechanisms and regulation
  • Autophagy in Disease and Therapy
  • Reproductive System and Pregnancy
  • Endometriosis Research and Treatment
  • Phagocytosis and Immune Regulation
  • Microtubule and mitosis dynamics
  • Metabolism and Genetic Disorders
  • Advanced battery technologies research
  • ATP Synthase and ATPases Research
  • Metabolism, Diabetes, and Cancer
  • Nutrition and Health in Aging
  • Inflammasome and immune disorders
  • Lysosomal Storage Disorders Research
  • Pregnancy and preeclampsia studies
  • Health, psychology, and well-being
  • Metalloenzymes and iron-sulfur proteins
  • Calcium signaling and nucleotide metabolism
  • Erythrocyte Function and Pathophysiology
  • Carbohydrate Chemistry and Synthesis
  • Biochemical Acid Research Studies
  • Neuroethics, Human Enhancement, Biomedical Innovations
  • Adipose Tissue and Metabolism

Universidad Pablo de Olavide
2011-2024

Centro Andaluz de Biología del Desarrollo
2011-2020

Centro de Investigación Biomédica en Red
2011-2018

Instituto de Salud Carlos III
2010-2018

Consejo Superior de Investigaciones Científicas
2011-2018

Instituto de Investigación de Enfermedades Raras
2018

Junta de Andalucía
2012-2017

Centre for Biomedical Network Research on Rare Diseases
2010-2015

Unidades Centrales Científico-Técnicas
2012

Coenzyme Q10 (CoQ) is a small lipophilic molecule critical for the transport of electrons from complexes I and II to complex III in mitochondrial respiratory chain. CoQ deficiency rare human genetic condition that has been associated with variety clinical phenotypes. With aim elucidating how affects an organism, we have investigated pathophysiologic processes present within fibroblasts derived 4 patients deficiency. Assays cultured revealed decreased activities II+III, III, IV, reduced...

10.4161/auto.5.1.7174 article EN Autophagy 2009-01-01

Abstract Introduction Fibromyalgia is a chronic pain syndrome with unknown etiology. Recent studies have shown some evidence demonstrating that oxidative stress may role in the pathophysiology of fibromyalgia. However, it still not clear whether cause or effect abnormalities documented Furthermore, mitochondria redox imbalance reported fibromyalgia also controversial. We undertook this study to investigate mitochondrial dysfunction, stress, and mitophagy Methods studied 20 patients (2 male,...

10.1186/ar2918 article EN cc-by Arthritis Research & Therapy 2010-01-28

For a number of years, coenzyme Q10 (CoQ10) was known for its key role in mitochondrial bioenergetics; later studies demonstrated presence other subcellular fractions and blood plasma, extensively investigated antioxidant role. These 2 functions constitute the basis supporting clinical use CoQ10. Also, at inner membrane level, CoQ10 is recognized as an obligatory cofactor function uncoupling proteins modulator transition pore. Furthermore, recent data indicate that affects expression genes...

10.1159/000360101 article EN Molecular Syndromology 2014-01-01

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) is a mitochondrial disease most usually caused by point mutations in tRNA genes encoded mtDNA. Here, we report on how this mutation affects function primary fibroblast cultures established from 2 patients with MELAS who harbored the A3243G mutation. Both respiratory chain enzyme activities coenzyme Q(10) (CoQ) levels were significantly decreased fibroblasts. A similar decrease membrane potential was found...

10.1096/fj.10-165340 article EN The FASEB Journal 2011-05-06

Abstract Gaucher disease (GD) is caused by mutations in the GBA1 gene, which encodes lysosomal β-glucocerebrosidase. Homozygosity for L444P mutation associated with high risk of neurological manifestations are not improved enzyme replacement therapy. Alternatively, pharmacological chaperones (PCs) capable restoring correct folding and trafficking mutant represent promising alternative therapies.Here, we report on how affects mitochondrial function primary fibroblast derived from GD patients....

10.1038/srep10903 article EN cc-by Scientific Reports 2015-06-05

MELAS (mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes) is a mitochondrial disease most usually caused by point mutations in tRNA genes encoded DNA (mtDNA). Approximately 80% of cases syndrome are associated with m.3243A > G mutation the MT-TL1 gene, which encodes tRNALeu (UUR). Currently, no effective treatments available for this chronic progressive disorder. Treatment strategies other diseases consist several drugs that diminish deleterious effects abnormal...

10.1111/j.1476-5381.2012.02086.x article EN British Journal of Pharmacology 2012-07-02

<h3>Background</h3> Fibromyalgia (FM) is a worldwide diffuse musculoskeletal chronic pain condition that affects up to 5% of the general population. Many symptoms associated with mitochondrial diseases are reported in patients FM such as exercise intolerance, fatigue, myopathy and dysfunction. In this study, we report mutation cytochrome b gene DNA (mtDNA) family inflammasome complex activation. <h3>Methods</h3> mtDNA from blood cells five were sequenced. We clinically genetically...

10.1136/jmedgenet-2015-103392 article EN Journal of Medical Genetics 2015-11-13

Apoptotic microtubule network (AMN) is organized during apoptosis, forming a cortical structure beneath plasma membrane, which has an important role in preserving cell morphology and membrane permeability. The aim of this study was to examine the AMN maintaining integrity execution phase apoptosis. We demonstrated camptothecin-induced apoptosis H460 cells that delimits active caspase free area permits preservation cellular cortex transmembrane proteins. depolymerization apoptotic by short...

10.1038/cddis.2013.58 article EN cc-by Cell Death and Disease 2013-03-07

Systemic treatments for hepatocellular carcinoma (HCC) have been largelyunsuccessful.This study investigated the antitumoral activity of Amitriptyline, a tricyclic antidepressant, in hepatoma cells.Amitriptyline-induced toxicity involved early mitophagy activation that subsequently switched to apoptosis.Amitriptyline induced mitochondria dysfunction and oxidative stress HepG2 cells.Amitriptyline specifically inhibited mitochondrial complex III is associated with decreased membrane potential...

10.18632/genesandcancer.114 article EN Genes & Cancer 2016-08-07
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