eprintid: 109 rev_number: 14 eprint_status: archive userid: 2 importid: 0 dir: disk0/00/00/01/09 datestamp: 2021-06-01 23:55:06 lastmod: 2023-07-10 23:30:16 status_changed: 2021-06-01 23:55:06 type: article succeeds: 0 commentary: 0 metadata_visibility: show item_issues_count: 0 sword_depositor: 0 creators_name: Rivas-García, Lorenzo creators_name: Quiles, José L. creators_name: Varela-López, Alfonso creators_name: Giampieri, Francesca creators_name: Battino, Maurizio creators_name: Bettmer, Jörg creators_name: Montes-Bayón, María creators_name: Llopis, Juan creators_name: Sánchez-González, Cristina creators_id: creators_id: jose.quiles@uneatlantico.es creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: title: Ultra-Small Iron Nanoparticles Target Mitochondria Inducing Autophagy, Acting on Mitochondrial DNA and Reducing Respiration ispublished: pub subjects: uneat_bm divisions: uneatlantico_produccion_cientifica full_text_status: public keywords: Copy number, Metals, Mitochondria, MtDNA deletions, Nanotechnology, Respiration. abstract: The application of metallic nanoparticles (materials with size at least in one dimension ranging from 1 to 100 nm) as a new therapeutic tool will improve the diagnosis and treatment of diseases. The mitochondria could be a therapeutic target to treat pathologies whose origin lies in mitochondrial dysfunctions or whose progression is dependent on mitochondrial function. We aimed to study the subcellular distribution of 2-4 nm iron nanoparticles and its effect on mitochondrial DNA (mtDNA), mitochondrial function, and autophagy in colorectal cell lines (HT-29). Results showed that when cells were exposed to ultra-small iron nanoparticles, their subcellular fate was mainly mitochondria, affecting its respiratory and glycolytic parameters, inducing the migration of the cellular state towards quiescence, and promoting and triggering the autophagic process. These effects support the potential use of nanoparticles as therapeutic agents using mitochondria as a target for cancer and other treatments for mitochondria-dependent pathologies. date: 2021-01 date_type: published publication: Pharmaceutics volume: 13 number: 1 pagerange: 90 pages: 0 id_number: doi:10.3390/pharmaceutics13010090 refereed: TRUE issn: 1999-4923 official_url: http://doi.org/10.3390/pharmaceutics13010090 num_pieces: 0 gscholar_impact: 0 gscholar_datestamp: 0000-00-00 00:00:00 access: open language: en citation: Artículo Materias > Biomedicina Universidad Europea del Atlántico > Investigación > Producción Científica Abierto Inglés The application of metallic nanoparticles (materials with size at least in one dimension ranging from 1 to 100 nm) as a new therapeutic tool will improve the diagnosis and treatment of diseases. The mitochondria could be a therapeutic target to treat pathologies whose origin lies in mitochondrial dysfunctions or whose progression is dependent on mitochondrial function. We aimed to study the subcellular distribution of 2-4 nm iron nanoparticles and its effect on mitochondrial DNA (mtDNA), mitochondrial function, and autophagy in colorectal cell lines (HT-29). Results showed that when cells were exposed to ultra-small iron nanoparticles, their subcellular fate was mainly mitochondria, affecting its respiratory and glycolytic parameters, inducing the migration of the cellular state towards quiescence, and promoting and triggering the autophagic process. These effects support the potential use of nanoparticles as therapeutic agents using mitochondria as a target for cancer and other treatments for mitochondria-dependent pathologies. metadata Rivas-García, Lorenzo; Quiles, José L.; Varela-López, Alfonso; Giampieri, Francesca; Battino, Maurizio; Bettmer, Jörg; Montes-Bayón, María; Llopis, Juan y Sánchez-González, Cristina mail SIN ESPECIFICAR, jose.quiles@uneatlantico.es, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR (2021) Ultra-Small Iron Nanoparticles Target Mitochondria Inducing Autophagy, Acting on Mitochondrial DNA and Reducing Respiration. Pharmaceutics, 13 (1). p. 90. ISSN 1999-4923 document_url: http://repositorio.uneatlantico.es/id/eprint/109/1/pharmaceutics-13-00090.pdf