ArticleNeurobiology of aging2016
Age increases reactive oxygen species production in macrophages and potentiates oxidative damage after spinal cord injury.
Article in Neurobiology of aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- The role of sex hormones in neurological and functional recovery following spinal cord injury in females: a systematic review of the literature.Spinal cord · 2026Pooled it
- Dynamic metabolic programming of monocyte-derived cells defines immunity in CNS disease.Brain : a journal of neurology · 2026Review
- Polydatin for treating spinal cord injury: Multiple mechanisms and challenges.Journal of pharmaceutical analysis · 2026Review
- Acrolein-Induced Alterations in Morphology and Stress Resilience in hiPSC-Derived Cortical Neurons.Environmental science & technology · 2025Article
- Nrf2 signaling pathway: focus on oxidative stress in osteoporosis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2025Review
- A Review of the Potential Use of Antioxidants in Spinal Cord Injuries.Antioxidants (Basel, Switzerland) · 2025Review
- Molecular pathology of acute spinal cord injury in middle-aged mice.Journal of neuroinflammation · 2025Article
- Spinal Cord Injury and Ageing: The Role of Chronic Neuroinflammation.Aging and disease · 2025Review
- Redefining macrophage phenotypes after spinal cord injury: An open data approach.Experimental neurology · 2025Article
- Nrf2 Signaling Pathway: Focus on Oxidative Stress in Spinal Cord Injury.Molecular neurobiology · 2025Review
- The Effect of Local Melatonin Application on Bone Fracture Healing in Rat Tibias.Medicina (Kaunas, Lithuania) · 2025Article
- Nonresolving Neuroinflammation Regulates Axon Regeneration in Chronic Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Pharmacological Network Analysis of the Functions and Mechanism of Quercetin From Jisuikang (JSK) in Spinal Cord Injury (SCI).Journal of cellular and molecular medicine · 2024Article
- Bibliometric analysis of the inflammation expression after spinal cord injury: current research status and emerging frontiers.Spinal cord · 2024Review
- Non-resolving neuroinflammation regulates axon regeneration in chronic spinal cord injury.bioRxiv : the preprint server for biology · 2024Article
- Biomimetic nanoplatform with anti-inflammation and neuroprotective effects for repairing spinal cord injury in mice.Materials today. Bio · 2023Article
- Prognostic Value of Malondialdehyde (MDA) in the Temporal Progression of Chronic Spinal Cord Injury.Journal of personalized medicine · 2023Article
- Effects of NADPH Oxidase Isoform-2 (NOX2) Inhibition on Behavioral Responses and Neuroinflammation in a Mouse Model of Neuropathic Pain.Biomedicines · 2023Article
- A Biomaterial Model to Assess the Effects of Age in Vascularization.Cells, tissues, organs · 2023Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Age potentiates neurodegeneration and impairs recovery from spinal cord injury (SCI). Previously, we observed that age alters the balance of destructive (M1) and protective (M2) macrophages; however, the age-related pathophysiology in SCI is poorly understood. Nicotinamide adenine dinucleotide phosphate oxidase (NOX) contributes to reactive oxygen species (ROS)-mediated damage and macrophage activation in neurotrauma. Further, NOX and ROS increase with central nervous system age. Here, we found significantly higher ROS generation in 14 versus 4-month-old (MO) mice after contusion SCI. Notably, NOX2 increased in 14 MO ROS-producing macrophages suggesting that macrophages and NOX contribute to SCI oxidative stress. Indicators of lipid peroxidation, a downstream cytotoxic effect of ROS accumulation, were significantly higher in 14 versus 4 MO SCI mice. We also detected a higher percentage of ROS-producing M2 (Arginase-1-positive) macrophages in 14 versus 4 MO mice, a previously unreported SCI phenotype, and increased M1 (CD16/32-positive) macrophages with age. Thus, NOX and ROS are age-related mediators of SCI pathophysiology and normally protective M2 macrophages may potentiate secondary injury through ROS generation in the aged injured spinal cord.
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.