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Trimetazidine Improves Mitochondrial Dysfunction in SOD1G93A Cellular Models of Amyotrophic Lateral...

Trimetazidine Improves Mitochondrial Dysfunction in SOD1G93A Cellular Models of Amyotrophic Lateral...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10970050

Trimetazidine Improves Mitochondrial Dysfunction in SOD1G93A Cellular Models of Amyotrophic Lateral Sclerosis through Autophagy Activation

About this item

Full title

Trimetazidine Improves Mitochondrial Dysfunction in SOD1G93A Cellular Models of Amyotrophic Lateral Sclerosis through Autophagy Activation

Publisher

Basel: MDPI AG

Journal title

International journal of molecular sciences, 2024-03, Vol.25 (6), p.3251

Language

English

Formats

Publication information

Publisher

Basel: MDPI AG

More information

Scope and Contents

Contents

Amyotrophic Lateral Sclerosis (ALS) is considered the prototype of motor neuron disease, characterized by motor neuron loss and muscle waste. A well-established pathogenic hallmark of ALS is mitochondrial failure, leading to bioenergetic deficits. So far, pharmacological interventions for the disease have proven ineffective. Trimetazidine (TMZ) is...

Alternative Titles

Full title

Trimetazidine Improves Mitochondrial Dysfunction in SOD1G93A Cellular Models of Amyotrophic Lateral Sclerosis through Autophagy Activation

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10970050

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10970050

Other Identifiers

ISSN

1422-0067,1661-6596

E-ISSN

1422-0067

DOI

10.3390/ijms25063251

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