Observational studyJournal of translational medicine2018
Exhaustion of mitochondrial and autophagic reserve may contribute to the development of LRRK2
Open access · goldAbstract readObservational Study
In one paragraph
Observational study in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18citing papers in PubMed
4.1field-weighted citation impact, top 6% of its field
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- LRRK2-mediated mitochondrial dysfunction in Parkinson's disease.The Biochemical journal · 2025Review
- Article
- Article
- Review
- Astrocytic atrophy as a pathological feature of Parkinson's disease with LRRK2 mutation.NPJ Parkinson's disease · 2021Article
- Synergistic Effects of Milk-Derived Exosomes and Galactose onInternational journal of molecular sciences · 2021Review
- A Conserved Role for LRRK2 and Roco Proteins in the Regulation of Mitochondrial Activity.Frontiers in cell and developmental biology · 2021Article
- Mitochondrial Defects in Fibroblasts of PathogenicFrontiers in cell and developmental biology · 2021Article
- Disrupted Mitochondrial and Metabolic Plasticity Underlie Comorbidity between Age-Related and Degenerative Disorders as Parkinson Disease and Type 2 Diabetes Mellitus.Antioxidants (Basel, Switzerland) · 2020Article
- Mitochondrial Determinants of Doxorubicin-Induced Cardiomyopathy.Circulation research · 2020Review
- Mitochondrial Mechanisms of LRRK2 G2019S Penetrance.Frontiers in neurology · 2020Article
- Galactose-Induced Skin Aging: The Role of Oxidative Stress.Oxidative medicine and cellular longevity · 2020Review
- LRRK2 and α-Synuclein: Distinct or Synergistic Players in Parkinson's Disease?Frontiers in neuroscience · 2020Review
- "LRRK2: Autophagy and Lysosomal Activity".Frontiers in neuroscience · 2020Review
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- LRRK2 is involved in the pathogenesis of system lupus erythematosus through promoting pathogenic antibody production.Journal of translational medicine · 2019Article
- Article
- Bioenergetics and Autophagic Imbalance in Patients-Derived Cell Models of Parkinson Disease Supports Systemic Dysfunction in Neurodegeneration.Frontiers in neuroscience · 2019Review
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Diana Luz Juárez-FloresLaboratory of Muscle Research and Mitochondrial Function-CELLEX, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Department of Internal Medicine-Hospital Clínic of Barcelona, Faculty of Medicine and Health Sciences, University of Barcelona (UB), Barcelona, Spain.ORCID 0000-0003-3615-7803
Ingrid González-CasacubertaLaboratory of Muscle Research and Mitochondrial Function-CELLEX, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Department of Internal Medicine-Hospital Clínic of Barcelona, Faculty of Medicine and Health Sciences, University of Barcelona (UB), Barcelona, Spain.
Mario EzquerraLaboratory of Parkinson disease and other Neurodegenerative Movement Disorders: Clinical and Experimental Research, Department of Neurology, Hospital Clínic of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona (UB), Barcelona, Spain.
María BañóLaboratory of Muscle Research and Mitochondrial Function-CELLEX, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Department of Internal Medicine-Hospital Clínic of Barcelona, Faculty of Medicine and Health Sciences, University of Barcelona (UB), Barcelona, Spain.
Francesc Carmona-PontaqueDepartment of Genetics, Microbiology and Statistics, University of Barcelona, Barcelona, Spain.
Marc Catalán-GarcíaLaboratory of Muscle Research and Mitochondrial Function-CELLEX, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Department of Internal Medicine-Hospital Clínic of Barcelona, Faculty of Medicine and Health Sciences, University of Barcelona (UB), Barcelona, Spain.
Mariona Guitart-MampelLaboratory of Muscle Research and Mitochondrial Function-CELLEX, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Department of Internal Medicine-Hospital Clínic of Barcelona, Faculty of Medicine and Health Sciences, University of Barcelona (UB), Barcelona, Spain.
Juan José RiveroLaboratory of Muscle Research and Mitochondrial Function-CELLEX, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Department of Internal Medicine-Hospital Clínic of Barcelona, Faculty of Medicine and Health Sciences, University of Barcelona (UB), Barcelona, Spain.
Ester TobiasLaboratory of Muscle Research and Mitochondrial Function-CELLEX, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Department of Internal Medicine-Hospital Clínic of Barcelona, Faculty of Medicine and Health Sciences, University of Barcelona (UB), Barcelona, Spain.
Jose Cesar MilisendaLaboratory of Muscle Research and Mitochondrial Function-CELLEX, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Department of Internal Medicine-Hospital Clínic of Barcelona, Faculty of Medicine and Health Sciences, University of Barcelona (UB), Barcelona, Spain.
Eduard TolosaLaboratory of Parkinson disease and other Neurodegenerative Movement Disorders: Clinical and Experimental Research, Department of Neurology, Hospital Clínic of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona (UB), Barcelona, Spain.
Maria Jose MartiLaboratory of Parkinson disease and other Neurodegenerative Movement Disorders: Clinical and Experimental Research, Department of Neurology, Hospital Clínic of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona (UB), Barcelona, Spain.
Ruben Fernández-SantiagoLaboratory of Parkinson disease and other Neurodegenerative Movement Disorders: Clinical and Experimental Research, Department of Neurology, Hospital Clínic of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona (UB), Barcelona, Spain.
Francesc CardellachLaboratory of Muscle Research and Mitochondrial Function-CELLEX, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Department of Internal Medicine-Hospital Clínic of Barcelona, Faculty of Medicine and Health Sciences, University of Barcelona (UB), Barcelona, Spain.
Constanza MorénLaboratory of Muscle Research and Mitochondrial Function-CELLEX, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Department of Internal Medicine-Hospital Clínic of Barcelona, Faculty of Medicine and Health Sciences, University of Barcelona (UB), Barcelona, Spain. cmoren1@clinic.ub.es.
Glòria GarrabouLaboratory of Muscle Research and Mitochondrial Function-CELLEX, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Department of Internal Medicine-Hospital Clínic of Barcelona, Faculty of Medicine and Health Sciences, University of Barcelona (UB), Barcelona, Spain. garrabou@clinic.ub.es.
Centre for Biomedical Network Research on Rare Diseases · ESBiomedical Research Networking Center on Neurodegenerative Diseases · ESUniversitat de Barcelona · ES
Funding
Fondo de Investigación Sanitaria (FIS) ISCII PI11/00462Fundación Cellex CP042187Suports a Grups de Recerca de la Generalitat de Catalunya 893/2017
Abstract
backgroundMutations in leucine rich repeat kinase 2 (LRRK2) are the most common cause of familial Parkinson's disease (PD). Mitochondrial and autophagic dysfunction has been described as etiologic factors in different experimental models of PD. We aimed to study the role of mitochondria and autophagy in LRRK2
methodsFibroblasts from six non-manifesting LRRK2
resultsA similar mitochondrial phenotype of NM-LRRK2
conclusionsEnhanced mitochondrial performance of NM-LRRK2
Indexed as
AutophagyAdultAgedFemaleHeterozygoteHumansLeucine-Rich Repeat Serine-Threonine Protein Kinase-2MaleMiddle AgedMitochondriaMitochondrial DynamicsMutationParkinson DiseasePhenotypeLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humanAutophagyFibroblastsG2019SGalactoseGlucoseLRRK2Mitochondrial dynamicsMitochondrial dysfunctionNon-manifesting carriersParkinson’s disease
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.