Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Pioglitazone and Deoxyribonucleoside Combination Treatment Increases Mitochondrial Respiratory Capacity in m.3243A>G MELAS Cybrid Cells.

International journal of molecular sciences - 20 Mar 2020

Burgin Harrison J, Lopez Sanchez M Isabel G, Smith Craig M, Trounce Ian A, McKenzie Matthew

Abstract excerpt

The lack of effective treatments for mitochondrial disease has seen the development of new approaches, including those that aim to stimulate mitochondrial biogenesis to boost ATP generation above a critical disease threshold. Here, we examine the effects of the peroxisome proliferator-activated receptor γ (PPARγ) activator pioglitazone (PioG), in combination with deoxyribonucleosides (dNs), on mitochondrial...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Respiration
Share to DNA, Mitochondrial

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Dosage

Share to Hybrid Cells

Share to MELAS Syndrome

Share to Mitochondria

Share to Oxidative Phosphorylation

Share to Pioglitazone

Source

Open in PubMed Open full text

Identifiers

PMID: 32244971
DOI: 10.3390/ijms21062139
PMCID: PMC7139379

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Pioglitazone and Deoxyribonucleoside Combination Treatment Increases Mitochondrial Respiratory Capacity in m.3243A>G MELAS Cybrid Cells.PMID 32244971Read ↗

Alterations in coenzyme Q10 status in a cybrid line harboring the 3243A>G mutation of mitochondrial DNA is associated with abnormal mitochondrial bioenergetics and dysregulated mitochondrial biogenesis.Semantic proximity Read ↗

Emerging therapies for mitochondrial diseases.Semantic proximity Read ↗

Metabolically induced heteroplasmy shifting and l-arginine treatment reduce the energetic defect in a neuronal-like model of MELAS.Semantic proximity Read ↗

Constitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243A>G mtDNA mutationSemantic proximity Read ↗

Constitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243 A > G mtDNA mutation.Semantic proximity Read ↗

Metabolic rescue in pluripotent cells from patients with mtDNA disease.Semantic proximity Read ↗

PGC-1α/β induced expression partially compensates for respiratory chain defects in cells from patients with mitochondrial disordersSemantic proximity Read ↗

Screening of effective pharmacological treatments for MELAS syndrome using yeasts, fibroblasts and cybrid models of the disease.Semantic proximity Read ↗

Inflexibility of AMPK-mediated metabolic reprogramming in mitochondrial diseaseSemantic proximity Read ↗

Cell-free mtDNA drives pyroptosis and inflammation in m.3243A>G mitochondrial disease modelsSemantic proximity Read ↗

microRNA-mediated differential expression of TRMU, GTPBP3 and MTO1 in cell models of mitochondrial-DNA diseases.Semantic proximity Read ↗

Identification and small molecule rescue of mitochondrial dysfunction phenotype which converges across Leigh Syndrome and Huntington’s Disease patient fibroblastsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.