ReviewNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2014
PKC in developmental hypothyroid rat brain.
Review in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Effect ofNutrients · 2022Article
- PKCγ promotes axonal remodeling in the cortico-spinal tract via GSK3β/β-catenin signaling after traumatic brain injury.Scientific reports · 2019Article
- Ferroptosis and Its Role in Diverse Brain Diseases.Molecular neurobiology · 2019Review
- Thyroid Hormone Disruption in the Fetal and Neonatal Rat: Predictive Hormone Measures and Bioindicators of Hormone Action in the Developing Cortex.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Renin-angiotensin system acting on reactive oxygen species in paraventricular nucleus induces sympathetic activation via AT1R/PKCγ/Rac1 pathway in salt-induced hypertension.Scientific reports · 2017Article
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
Thyroid hormone (TH) is essential for the proper development of mammalian central nervous system. TH deficiency during the critical period of brain development results in permanent cognitive and neurological impairments. Members of the protein kinase C (PKC) family play a key role in the regulation of cellular functions in the nervous system. Alteration of PKC can be involved in the pathogenesis of neuronal disorders. This review details recent progress made in determining the roles played by PKC isoforms in developing hypothyroid rat brain. Evidence indicates that hippocampus down-regulation of PKCβ and PKCγ may be related to impaired learning and memory observed in perinatal hypothyroid rats. Enhanced PKCα activity in neonatal hypothyroid brain may bring about oxidative stress and cause brain damage. The activated pro-apoptotic PKCs including PKCδ can cause extensive apoptosis in the hypothyroid rat brain.
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.