ArticleAging2015
PGC-1α controls mitochondrial biogenesis and dynamics in lead-induced neurotoxicity.
Article in Aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 64 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
64 citing papers in PubMed, 119 citations in OpenAlex.
- Molecular Basis of Ferroptosis and Pyroptosis in Lead-Induced Neurotoxicity: A Narrative Review of Current Evidence and Therapeutic Implications.Biological trace element research · 2026Review
- Mitochondrial regulation of brain development: evidence from zebrafish models.Fish physiology and biochemistry · 2026Review
- Pioglitazone Ameliorates Mitochondrial Oxidative Stress and Inflammation via AMPK-Dependent Inhibition of Mitochondrial Fission in Leigh Syndrome.Cell proliferation · 2026Article
- Novel small molecule derivatives improve survivability in the cellular model of Huntington's diseaseRSC medicinal chemistry · 2026Article
- Mitochondrial dysfunction in Alzheimer's disease and related sex differences.Frontiers in aging neuroscience · 2026Review
- Disturbances in Mitochondrial Network, Biogenesis, and Mitochondria-Mediated Inflammatory Responses in Selected Brain Structures of Rats Exposed to Lead (Pb) During Prenatal and Neonatal Development.International journal of molecular sciences · 2025Article
- Anandamide-Induced Neuroprotection of Cortical Neurons Relies on Metabolic/Redox Regulation and Mitochondrial Dynamics.Molecular neurobiology · 2025Article
- Modulation of Nrf2 and Mitochondrial Function: Pharmacological Implications.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Mitochondrial-based therapies for neurodegenerative diseases: a review of the current literature.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- PMCell biochemistry and biophysics · 2025Article
- Association of PPARGC1A gene polymorphism and mtDNA methylation with coal-burning fluorosis: a case-control study.BMC genomics · 2024Article
- Progesterone (P4) ameliorates cigarette smoke-induced chronic obstructive pulmonary disease (COPD).Molecular medicine (Cambridge, Mass.) · 2024Article
- Case-inspired exploration of renin mutations in autosomal dominant tubulointerstitial kidney disease: not all paths lead to the endoplasmic reticulum.Pediatric nephrology (Berlin, Germany) · 2024Article
- Review
- Yucca schidigera Extract Mitigates the Oxidative Damages, Inflammation, and Neurochemical Impairments in the Brains of Quails Exposed to Lead.Biological trace element research · 2024Article
- Exploring the potential roles of apelin, visfatin, and irisin in energy regulation in farm animals: an overview.Frontiers in veterinary science · 2024Review
- Modulating Mitochondrial Dynamics Mitigates Cognitive Impairment in Rats with Myocardial Infarction.Current neuropharmacology · 2024Article
- Increased cytotoxicity of PbEnvironmental science. Processes & impacts · 2023Article
- Mitochondrial dynamics in health and disease: mechanisms and potential targets.Signal transduction and targeted therapy · 2023Review
- Strong associations of telomere length and mitochondrial copy number with suicidality and abuse history in adolescent depressed individuals.Molecular psychiatry · 2023Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
- Erratum issued
- Erratum issued
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Due to its role in regulation of mitochondrial function, PGC1α is emerging as an important player in ageing and neurodegenerative disorders. PGC1α exerts its neuroprotective effects by promoting mitochondrial biogenesis (MB) and functioning. However, the precise regulatory role of PGC1α in the control of mitochondrial dynamics (MD) and neurotoxicity is still unknown. Here we elucidate the role of PGC1αin vitro and in vivo in the regulatory context of MB and MD in response to lead (II) acetate as a relevant model of neurotoxicity. We show that there is an adaptive response (AR) to lead, orchestrated by the BAP31-calcium signalling system operating between the ER and mitochondria. We find that this hormetic response is controlled by a cell-tolerated increase of PGC1α expression, which in turn induces a balanced expression of fusion/fission genes by binding to their promoters and implying its direct role in regulation of MD. However, dysregulation of PGC1α expression through either stable downregulation or overexpression, renders cells more susceptible to lead insult leading to mitochondrial fragmentation and cell death. Our data provide novel evidence that PGC1α expression is a key regulator of MD and the maintenance of tolerated PGC1α expression may offer a promising strategy for neuroprotective therapies.
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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.