ReviewJournal of the Association for Research in Otolaryngology : JARO2022
Cochlear Immune Response in Presbyacusis: a Focus on Dysregulation of Macrophage Activity.
Review in Journal of the Association for Research in Otolaryngology : JARO, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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
26 citing papers in PubMed, 30 citations in OpenAlex.
- Transient Sleep Deprivation Induces Persistent Auditory Neuropathy via ROS-Initiated Neuroinflammation and BK Channel Suppression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A prognostic nomogram for all frequencies sudden sensorineural hearing loss based on the commixed index of inflammatory-immune-hemostasis-nutrition.Scientific reports · 2026Article
- A Novel Central-Peripheral Interface: The Auditory Nerve Glial Transition Zone Exhibits Enhanced Age-Related Immune and Glial Cell Dysfunction.bioRxiv : the preprint server for biology · 2026Article
- [Research progress on the mechanism of auditory center remodeling and clinical intervention strategies in presbycusis].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2026Review
- XKR8 Deletion Protects Against Noise-Induced Hearing Loss by Attenuating Apoptosis and Preserving Mitochondrial Bioenergetics in the Cochlea.Molecular neurobiology · 2026Article
- The auditory nerve glial transition zone is a focal site of age-related immune-myelin interactions.Frontiers in immunology · 2026Article
- Cochlear macrophage CD74 enhances the apoptosis of senescent cochlear hair cells by down-regulating MIF.Frontiers in immunology · 2026Article
- Cochlear Inflammatory Microenvironment in Age-Related Hearing Loss: Mechanisms and Recent Advances.Clinical interventions in aging · 2026Review
- Sentinels or saboteurs, the Janus face of cochlear-resident macrophages in hearing loss: spatiotemporal distribution, pathophysiological functions, and translational potential.Journal of neuroinflammation · 2025Review
- Comprehensive analysis of aberrant alternative splicing and RNA binding proteins associated with age-related sensorineural hearing loss.Scientific reports · 2025Article
- Differential expression and regulation of FASLG by miR-5195/miR-3941 in age-related hearing loss.PloS one · 2025Article
- Cochlear immunology and its therapeutic revolution.Frontiers in immunology · 2025Review
- Age-related changes in the zebrafish and killifish inner ear and lateral line.Scientific reports · 2024Article
- Article
- Mitochondrial Regulation of Macrophages in Innate Immunity and Diverse Roles of Macrophages During Cochlear Inflammation.Neuroscience bulletin · 2024Review
- Oxidative stress and inflammation cause auditory system damage via glial cell activation and dysregulated expression of gap junction proteins in an experimental model of styrene-induced oto/neurotoxicity.Journal of neuroinflammation · 2024Article
- A critical evaluation of "leakage" at the cochlear blood-stria-barrier and its functional significance.Frontiers in molecular neuroscience · 2024Review
- The Stria Vascularis in Mice and Humans Is an Early Site of Age-Related Cochlear Degeneration, Macrophage Dysfunction, and Inflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Cochlear inflammaging: cellular and molecular players of the innate and adaptive immune system in age-related hearing loss.Frontiers in neurology · 2023Review
- Progress on mechanisms of age-related hearing loss.Frontiers in neuroscience · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Age-related hearing loss, or presbyacusis, is a prominent chronic degenerative disorder that affects many older people. Based on presbyacusis pathology, the degeneration occurs in both sensory and non-sensory cells, along with changes in the cochlear microenvironment. The progression of age-related neurodegenerative diseases is associated with an altered microenvironment that reflects chronic inflammatory signaling. Under these conditions, resident and recruited immune cells, such as microglia/macrophages, have aberrant activity that contributes to chronic neuroinflammation and neural cell degeneration. Recently, researchers identified and characterized macrophages in human cochleae (including those from older donors). Along with the age-related changes in cochlear macrophages in animal models, these studies revealed that macrophages, an underappreciated group of immune cells, may play a critical role in maintaining the functional integrity of the cochlea. Although several studies deciphered the molecular mechanisms that regulate microglia/macrophage dysfunction in multiple neurodegenerative diseases, limited studies have assessed the mechanisms underlying macrophage dysfunction in aged cochleae. In this review, we highlight the age-related changes in cochlear macrophage activities in mouse and human temporal bones. We focus on how complement dysregulation and the nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 inflammasome could affect macrophage activity in the aged peripheral auditory system. By understanding the molecular mechanisms that underlie these regulatory systems, we may uncover therapeutic strategies to treat presbyacusis and other forms of sensorineural hearing loss.
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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.