Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Gainutdinov 2022 BEC

From Bioblast


Bioenergetics Communications        
Gnaiger 2020 BEC MitoPathways
       
Gnaiger Erich et al ― MitoEAGLE Task Group (2020) Mitochondrial physiology. Bioenerg Commun 2020.1.
        MitoPedia: BEC         MitoPedia: Gentle Science         MitoFit Preprints         DOI Data Center
Bioenergetics Communications
Publications in the MiPMap
Gainutdinov T, Debska-Vielhaber G, Gizatullina Z, Vielhaber S, Orynbayeva Z, Gellerich FN (2022) Impaired Ca2+ signaling indicates disturbed mitochondrial function in fibroblasts from patients with sporadic and familial ALS. Bioenerg Commun 2022.18. https://doi.org/10.26124/bec:2022-0018

Β» Bioenerg Commun 2022.18. Open Access pdf
published online 2022-12-09

AGainutdinov Timur, Debska-Vielhaber Grazyna, Gizatullina Zemfira, Vielhaber Stefan, Orynbayeva Zulfiya, Gellerich Frank Norbert (2022) Bioenerg Commun

Abstract: BEC.png https://doi.org/10.26124/bec:2022-0018
Amyotrophic lateral sclerosis (ALS) is a progressive, devastating, neurodegenerative disorder affecting upper and lower motor neurons. Common mechanisms of ALS pathogenesis disturb cellular calcium homeostasis and cause mitochondrial dysfunction. Both influence mutually each other. As a result, chronic mitochondrial energy stress impairs cellular signaling and transport processes, leading to degeneration of motor neurons. We measured cytosolic Ca2+ in healthy and ALS fibroblasts. Mitochondrial calcium retention capacity in fibroblasts obtained from patients with sporadic (sALS) and familial (fALS) ALS differed between two subtypes and from healthy individuals. Changes of [Ca2+]cyt dynamics in ALS fibroblasts was partially rescued by treatment with antioxidants (Trolox and CoQ10). These results confirm a causative role of oxidative stress in mitochondrial dysfunction linked to ALS.
β€’ Keywords: ALS, CoQ10, cellular Ca2+ homeostasis, histamine, mitochondria, Trolox β€’ Bioblast editor: Tindle-Solomon L β€’ O2k-Network Lab: DE Bonn Kunz WS, DE Magdeburg Debska-Vielhaber G, DE Magdeburg Gellerich FN

ORCID: ORCID.png Gainutdinov Timur, ORCID.png Debska-Vielhaber Grazyna, ORCID.png Gizatullina Zemfira, ORCID.png Vielhaber Stefan, ORCID.png Orynbayeva Zulfiya, ORCID.png Gellerich Frank Norbert

MitoFit Preprint

Β» Gainutdinov 2022 MitoFit


Labels: MiParea: Patients  Pathology: Inherited, Neurodegenerative 

Organism: Human  Tissue;cell: Fibroblast  Preparation: Intact cells 

Regulation: Calcium 



BEC