Next Article in Journal
Involvement of TREK-1 Channel in Cell Viability of H9c2 Rat Cardiomyoblasts Affected by Bupivacaine and Lipid Emulsion
Previous Article in Journal
Irisin and Bone: From Preclinical Studies to the Evaluation of Its Circulating Levels in Different Populations of Human Subjects
Previous Article in Special Issue
Gait Training in Virtual Reality: Short-Term Effects of Different Virtual Manipulation Techniques in Parkinson’s Disease
Article Menu

Article Versions

Export Article

Open AccessFeature PaperArticle

Synergistic Effect of Mitochondrial and Lysosomal Dysfunction in Parkinson’s Disease

Department of Biological and Environmental Sciences and Technologies (DiSTeBA), University of Salento, Via Provinciale Lecce-Monteroni 165, 73100 Lecce, Italy
Department of Medical and Surgical Sciences (DIMEC), Medical Genetics Unit, University of Bologna, via Massarenti 9, 40138 Bologna, Italy
Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy
Department of Basic Medical Sciences, Neurosciences and Sensory Organs, University of Bari "A. Moro", 70122 Bari, Italy
Authors to whom correspondence should be addressed.
Cells 2019, 8(5), 452;
Received: 23 March 2019 / Revised: 30 April 2019 / Accepted: 13 May 2019 / Published: 14 May 2019
(This article belongs to the Special Issue The Molecular and Cellular Basis for Parkinson's Disease 2019)
PDF [3056 KB, uploaded 14 May 2019]


Crosstalk between lysosomes and mitochondria plays a central role in Parkinson’s Disease (PD). Lysosomal function may be influenced by mitochondrial quality control, dynamics and/or respiration, but whether dysfunction of endocytic or autophagic pathway is associated with mitochondrial impairment determining accumulation of defective mitochondria, is not yet understood. Here, we performed live imaging, western blotting analysis, sequencing of mitochondrial DNA (mtDNA) and senescence-associated beta-galactosidase activity assay on primary fibroblasts from a young patient affected by PD, her mother and a healthy control to analyze the occurrence of mtDNA mutations, lysosomal abundance, acidification and function, mitochondrial biogenesis activation and senescence. We showed synergistic alterations in lysosomal functions and mitochondrial biogenesis, likely associated with a mitochondrial genetic defect, with a consequent block of mitochondrial turnover and occurrence of premature cellular senescence in PARK2-PD fibroblasts, suggesting that these alterations represent potential mechanisms contributing to the loss of dopaminergic neurons.
Keywords: Parkinson’s disease; lysosome; autophagy; endocytosis; mitochondria Parkinson’s disease; lysosome; autophagy; endocytosis; mitochondria
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Guerra, F.; Girolimetti, G.; Beli, R.; Mitruccio, M.; Pacelli, C.; Ferretta, A.; Gasparre, G.; Cocco, T.; Bucci, C. Synergistic Effect of Mitochondrial and Lysosomal Dysfunction in Parkinson’s Disease. Cells 2019, 8, 452.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Cells EISSN 2073-4409 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top