ReviewAging cell2007
Age-dependent changes in Ca2+ homeostasis in peripheral neurones: implications for changes in function.
Review in Aging cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 48 citations in OpenAlex.
- Sympathetic motor neuron dysfunction is a missing link in age-associated sympathetic overactivity.eLife · 2024Article
- Sympathetic Motor Neuron Dysfunction is a Missing Link in Age-Associated Sympathetic Overactivity.bioRxiv : the preprint server for biology · 2024Article
- Association between serum calcium and prognosis in patients with acute ischemic stroke in ICU: analysis of the MIMIC-IV database.BMC anesthesiology · 2024Article
- The inter-chamber differences in the contractile function between left and right atrial cardiomyocytes in atrial fibrillation in rats.Frontiers in cardiovascular medicine · 2023Article
- Review
- Review
- Sorcin is an early marker of neurodegeneration, CaCell death & disease · 2020Article
- Resveratrol Directly Controls the Activity of Neuronal Ryanodine Receptors at the Single-Channel Level.Molecular neurobiology · 2020Article
- The Puzzling Role of Neuron-Specific PMCA Isoforms in the Aging Process.International journal of molecular sciences · 2019Review
- Neural activity regulates autoimmune diseases through the gateway reflex.Bioelectronic medicine · 2019Review
- Mechanisms Through Which Some Mitochondria-Generated Metabolites Act as Second Messengers That Are Essential Contributors to the Aging Process in Eukaryotes Across Phyla.Frontiers in physiology · 2019Review
- Vitamin D deficiency accelerates ageing and age-related diseases: a novel hypothesis.The Journal of physiology · 2017Review
- Impact of Aging on Calcium Signaling and Membrane Potential in Endothelium of Resistance Arteries: A Role for Mitochondria.The journals of gerontology. Series A, Biological sciences and medical sciences · 2017Article
- Recognition and control of the progression of age-related hearing loss.Rejuvenation research · 2013Review
- Mitochondrial DNA oxidative damage and repair in aging and Alzheimer's disease.Antioxidants & redox signaling · 2013Review
- Double-blind, placebo-controlled, two-period, crossover trial to examine the pharmacokinetics of lisdexamfetamine dimesylate in healthy older adults.Neuropsychiatric disease and treatment · 2013Article
- Spreading the signal for vasodilatation: implications for skeletal muscle blood flow control and the effects of ageing.The Journal of physiology · 2012Review
- Age-associated loss of selectivity in human olfactory sensory neurons.Neurobiology of aging · 2012Article
- Abnormal intracellular calcium homeostasis in sympathetic neurons from young prehypertensive rats.Hypertension (Dallas, Tex. : 1979) · 2012Article
- Recent advances in the study of age-related hearing loss: a mini-review.Gerontology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Calcium ions represent universal second messengers within neuronal cells integrating multiple cellular functions, such as release of neurotransmitters, gene expression, proliferation, excitability, and regulation of cell death or apoptotic pathways. The magnitude, duration and shape of stimulation-evoked intracellular calcium ([Ca2+]i) transients are determined by a complex interplay of mechanisms that modulate stimulation-evoked rises in [Ca2+]i that occur with normal neuronal function. Disruption of any of these mechanisms may have implications for the function and health of peripheral neurones during the aging process. This review focuses on the impact of advancing age on the overall function of peripheral adrenergic neurones and how these changes in function may be linked to age-related changes in modulation of [Ca2+]i regulation. The data in this review suggest that normal aging in peripheral autonomic neurones is a subtle process and does not always result in dramatic deterioration in their function. We present studies that support the idea that in order to maintain cell viability peripheral neurones are able to compensate for an age-related decline in the function of at least one of the neuronal calcium-buffering systems, smooth endoplasmic reticulum calcium ATPases, by increased function of other calcium-buffering systems, namely, the mitochondria and plasmalemma calcium extrusion. Increased mitochondrial calcium uptake may represent a 'weak point' in cellular compensation as this over time may contribute to cell death. In addition, we present more recent studies on [Ca2+]i regulation in the form of the modulation of release of calcium from smooth endoplasmic reticulum calcium stores. These studies suggest that the contribution of the release of calcium from smooth endoplasmic reticulum calcium stores is altered with age through a combination of altered ryanodine receptor levels and modulation of these receptors by neuronal nitric oxide containing neurones.
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.