ReviewBritish journal of pharmacology2014
Turn up the power - pharmacological activation of mitochondrial biogenesis in mouse models.
Review in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
80 citing papers in PubMed, 142 citations in OpenAlex.
- Trial
- Integrated analysis of the involvement of nitric oxide synthesis in mitochondrial proliferation, mitochondrial deficiency and apoptosis in skeletal muscle fibres.Scientific reports · 2016Trial
- Norepinephrine regulates hippocampal mitochondrial biogenesis via β2-adrenergic receptor signaling and PGC-1α.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- MOTS-c preserves mitochondrial subpopulation bioenergetics and genome integrity to attenuate cardiac ischemia reperfusion injury.Molecular biology reports · 2026Article
- Exploring mitochondrial functions and dysfunctions in chondrocytes: toward the identification of novel therapies for osteoarthritis.Bone research · 2026Review
- Therapeutic potential of mitochondrial transfer in reversing mutant-to-wild-type mtDNA ratio and improving mitochondrial dysfunction in 1555A>G mtDNA mutation-associated hearing loss.Scientific reports · 2026Article
- Nutraceutical Interception of Cachexia: Grape-Derived Compounds as Pathophysiological Network Modulators.Biology · 2025Review
- Potentiation of mitochondrial function by mitoDREADD-GNature neuroscience · 2025Article
- Intermittent Fasting as a Neuroprotective Strategy: Gut-Brain Axis Modulation and Metabolic Reprogramming in Neurodegenerative Disorders.Nutrients · 2025Review
- Therapies for Mitochondrial Disease: Past, Present, and Future.Journal of inherited metabolic disease · 2025Review
- Protective effect of sinomenine against CCl4-induced acute liver injury through regulation of mitochondrial biogenesis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Peroxisome proliferator‑activated receptor γ coactivator‑1α in heart disease (Review).Molecular medicine reports · 2025Review
- Unraveling the role of mitochondrial dysfunction in diabetic kidney disease: insights and interventions.Frontiers in pharmacology · 2025Review
- Comparative study on muscle function in two different streptozotocin-induced diabetic models.Acta diabetologica · 2024Article
- Cellular and Molecular Responses to Mitochondrial DNA Deletions in Kearns-Sayre Syndrome: Some Underlying Mechanisms.Molecular neurobiology · 2024Review
- Pre-IVM with C-type natriuretic peptide promotes mitochondrial biogenesis of bovine oocytes via activation of CREB.Scientific reports · 2024Article
- [Preparation of peptide-functionalized affinity materials for the highly specific capture and analysis of mitochondria].Se pu = Chinese journal of chromatography · 2024Article
- Mitochondrial quality control in human health and disease.Military Medical Research · 2024Review
- Lipodystrophy in methylmalonic acidemia associated with elevated FGF21 and abnormal methylmalonylation.JCI insight · 2024Article
- Bezafibrate confers neuroprotection in the 5xFAD mouse model of Alzheimer's disease.Biochimica et biophysica acta. Molecular basis of disease · 2023Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The oxidative phosphorylation (OXPHOS) system in mitochondria is responsible for the generation of the majority of cellular energy in the form of ATP. Patients with genetic OXPHOS disorders form the largest group of inborn errors of metabolism. Unfortunately, there is still a lack of efficient therapies for these disorders other than management of symptoms. Developing therapies has been complicated because, although the total group of OXPHOS patients is relatively large, there is enormous clinical and genetic heterogeneity within this patient population. Thus there has been a lot of interest in generating relevant mouse models for the different kinds of OXPHOS disorders. The most common treatment strategies tested in these mouse models have aimed to up-regulate mitochondrial biogenesis, in order to increase the residual OXPHOS activity present in affected animals and thereby to ameliorate the energy deficiency. Drugs such as bezafibrate, resveratrol and AICAR target the master regulator of mitochondrial biogenesis PGC-1α either directly or indirectly to manipulate mitochondrial metabolism. This review will summarize the outcome of preclinical treatment trials with these drugs in mouse models of OXPHOS disorders and discuss similar treatments in a number of mouse models of common diseases in which pathology is closely linked to mitochondrial dysfunction. In the majority of these studies the pharmacological activation of the PGC-1α axis shows true potential as therapy; however, other effects besides mitochondrial biogenesis may be contributing to this as well.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.