2026-04-18T14:00:05Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/166382024-09-27T07:58:22Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Sierra-Magro, Ana
author
Bartolome, Fernando
author
Lozano-Muñoz, David
author
Alarcón-Gil, Jesús
author
Gine, Elena
author
Sanz-SanCristobal, Marina
author
Alonso-Gil, Sandra
author
Cortes-Canteli, Marta
author
Carro, Eva
author
Pérez-Castillo, Ana
author
Morales-García, José A
funder
Ministerio de Economía y Competitividad (España)
funder
Fundación Banco Santander
funder
Instituto de Salud Carlos III
funder
Centro de Investigación Biomédica en Red - CIBERNED (Enfermedades Neurodegenerativas)
2023-11-06T11:06:42Z
2023-11-06T11:06:42Z
2023-01-11
Int J Mol Sci. 2023 Jan 11;24(2):1459.
http://hdl.handle.net/20.500.12105/16638
36674978
10.3390/ijms24021459
1422-0067
International journal of molecular sciences
Parkinson's disease (PD) is a neurodegenerative disorder that results from the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Since there are only symptomatic treatments available, new cellular and molecular targets involved in the onset and progression of this disease are needed to develop effective treatments. CCAAT/Enhancer Binding Protein β (C/EBPβ) transcription factor levels are altered in patients with a variety of neurodegenerative diseases, suggesting that it may be a good therapeutic target for the treatment of PD. A list of genes involved in PD that can be regulated by C/EBPβ was generated by the combination of genetic and in silico data, the mitochondrial transcription factor A (TFAM) being among them. In this paper, we observed that C/EBPβ overexpression increased TFAM promoter activity. However, downregulation of C/EBPβ in different PD/neuroinflammation cellular models produced an increase in TFAM levels, together with other mitochondrial markers. This led us to propose an accumulation of non-functional mitochondria possibly due to the alteration of their autophagic degradation in the absence of C/EBPβ. Then, we concluded that C/EBPβ is not only involved in harmful processes occurring in PD, such as inflammation, but is also implicated in mitochondrial function and autophagy in PD-like conditions.
eng
C/EBPβ Regulates TFAM Expression, Mitochondrial Function and Autophagy in Cellular Models of Parkinson's Disease.
journal article
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C_EBPβ Regulates TFAM Expression_Int J Mol Sci_2023.pdf
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C_EBPβ Regulates TFAM Expression_Int J Mol Sci_2023.pdf.txt