Generation of mitochondrial reactive oxygen species is controlled by ATPase inhibitory factor 1 and regulates cognition

Autor: Esparza-Moltó PB, Romero-Carramiñana I, Núñez de Arenas C, Pereira MP, Blanco N, Pardo B, Bates GR, Sánchez-Castillo C, Artuch-Iriberri R, Murphy MP, Esteban JA, Cuezva JM

Publikováno v: Plos Biology
r-FSJD: Repositorio Institucional de Producción Científica de la Fundació Sant Joan de Déu
Fundació Sant Joan de Déu
r-FSJD. Repositorio Institucional de Producción Científica de la Fundació Sant Joan de Déu
Universidad de Alicante (UA)

The mitochondrial ATP synthase emerges as key hub of cellular functions controlling the production of ATP, cellular signaling, and fate. It is regulated by the ATPase inhibitory factor 1 (IF1), which is highly abundant in neurons. Herein, we ablated

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=dedup_wf_001::50d8658ebd9bc37da9db4f4d07ab260b
http://fundanet.fsjd.org/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=19602

Targeting mitochondrial oxidative stress with MitoQ reduces NET formation and kidney disease in lupus-prone MRL-lpr mice

Autor: Fortner, KA, Blanco, Luz P., Buskiewicz, I, Huang, N, Gibson, PC, Cook, DL, Pedersen, Hege Lynum, Yuen, PST, Murphy, MP, Perl, A, Kaplan, Mariana J., Budd, RC

Publikováno v: Fortner, Blanco LP, Buskiewicz, Huang N, Gibson, Cook, Pedersen hl, Yuen, Murphy, Perl, Kaplan MJ, Budd. Targeting mitochondrial oxidative stress with MitoQ reduces NET formation and kidney disease in lupus-prone MRL-lpr mice.. Lupus Science and Medicine. 2020

Externí odkaz: https://hdl.handle.net/10037/18628

The Mitochondria-Targeted Antioxidant MitoQ Modulates Mitochondrial Function and Endoplasmic Reticulum Stress in Pancreatic ß Cells Exposed to Hyperglycaemia

Autor: Escribano-Lopez I, Bañuls C, Diaz-Morales N, Iannantuoni F, Rovira-Llopis S, Gomis R, Rocha M, Hernandez-Mijares A, Murphy MP, Victor VM

Publikováno v: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
r-FISABIO: Repositorio Institucional de Producción Científica
Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana (FISABIO)
r-FISABIO. Repositorio Institucional de Producción Científica
instname
r-INCLIVA. Repositorio Institucional de Producción Científica de INCLIVA

Mitochondria-targeted antioxidants such as mitoquinone (MitoQ) have demonstrated protective effects against oxidative damage in several diseases. The increase in reactive oxygen species (ROS) production during glucose metabolism in ß cells can be ex

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=dedup_wf_001::a15f3e71e8ea61ffa0bd0a85e1fe6a23
https://fundanet.fisabio.san.gva.es/publicaciones/ProdCientif/PublicacionFrw.aspx?id=3294

Trisomy of human chromosome 21 enhances amyloid-β deposition independently of an extra copy of APP

Autor: Wiseman, FK, Pulford, LJ, Barkus, C, Liao, F, Portelius, E, Webb, R, Chávez-Gutiérrez, L, Cleverley, K, Noy, S, Sheppard, O, Collins, T, Powell, C, Sarell, CJ, Rickman, M, Choong, X, Tosh, JL, Siganporia, C, Whittaker, HT, Stewart, F, Szaruga, M, London Down syndrome consortium, Murphy, MP, Blennow, K, De Strooper, B, Zetterberg, H, Bannerman, D, Holtzman, DM, Tybulewicz, VLJ, Fisher, EMC

Down syndrome, caused by trisomy of chromosome 21, is the single most common risk factor for early-onset Alzheimer's disease. Worldwide approximately 6 million people have Down syndrome, and all these individuals will develop the hallmark amyloid pla

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=od______1032::05b228e35b005f50a833e700e8910ccb
http://hdl.handle.net/10044/1/60437

Mitochondrial respiration is reduced in atherosclerosis, promoting necrotic core formation and reducing relative fibrous cap thickness

Autor: Bennett, MR, Yu, EPK, Reinhold, Starks, L, Uryga, Foote, Finigan, A, Figg, N, Pung, Y-F, Logan, A, Murphy, MP

Objective: Mitochondrial DNA (mtDNA) damage is present in murine and human atherosclerotic plaques. However, whether endogenous levels of mtDNA damage are sufficient to cause mitochondrial dysfunction, and whether decreasing mtDNA damage and improvin

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::93189bec7acd1839336dfbed29c2f5c4
https://www.repository.cam.ac.uk/handle/1810/274895