ArticleFrontiers in aging neuroscience2020
Guanylyl Cyclase A/cGMP Signaling Slows Hidden, Age- and Acoustic Trauma-Induced Hearing Loss.
Article in Frontiers in aging neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Trends and mechanistic insights into hypertension-associated hearing loss: a 20-year perspective (2005-2025).Frontiers in molecular neuroscience · 2026Pooled it
- Altered Auditory Maturation in Fragile X Syndrome and Its Involvement in Audiogenic Seizure Susceptibility.Autism research : official journal of the International Society for Autism Research · 2026Article
- PJ34 prevents cisplatin-induced hair cell loss via inhibition of PARP-1-AIF parthanatos.Biomolecules & biomedicine · 2025Article
- Acute deletion of the central MR/GR steroid receptor correlates with changes in LTP, auditory neural gain, and GC-A cGMP signaling.Frontiers in molecular neuroscience · 2023Article
- Article
- A potassium channel agonist protects hearing function and promotes outer hair cell survival in a mouse model for age-related hearing loss.Cell death & disease · 2022Article
- Loss of central mineralocorticoid or glucocorticoid receptors impacts auditory nerve processing in the cochlea.iScience · 2022Article
- Stress Affects Central Compensation of Neural Responses to Cochlear Synaptopathy in a cGMP-Dependent Way.Frontiers in neuroscience · 2022Article
- Age-related hearing loss pertaining to potassium ion channels in the cochlea and auditory pathway.Pflugers Archiv : European journal of physiology · 2021Review
- Activation of KCNQ4 as a Therapeutic Strategy to Treat Hearing Loss.International journal of molecular sciences · 2021Review
- Age-Dependent Auditory Processing Deficits after Cochlear Synaptopathy Depend on Auditory Nerve Latency and the Ability of the Brain to Recruit LTP/BDNF.Brain sciences · 2020Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the inner ear, cyclic guanosine monophosphate (cGMP) signaling has been described as facilitating otoprotection, which was previously observed through elevated cGMP levels achieved by phosphodiesterase 5 inhibition. However, to date, the upstream guanylyl cyclase (GC) subtype eliciting cGMP production is unknown. Here, we show that mice with a genetic disruption of the gene encoding the cGMP generator GC-A, the receptor for atrial and B-type natriuretic peptides, display a greater vulnerability of hair cells to hidden hearing loss and noise- and age-dependent hearing loss. This vulnerability was associated with GC-A expression in spiral ganglia and outer hair cells (OHCs) but not in inner hair cells (IHCs). GC-A knockout mice exhibited elevated hearing thresholds, most pronounced for the detection of high-frequency tones. Deficits in OHC input-output functions in high-frequency regions were already present in young GC-A-deficient mice, with no signs of an accelerated progression of age-related hearing loss or higher vulnerability to acoustic trauma. OHCs in these frequency regions in young GC-A knockout mice exhibited diminished levels of KCNQ4 expression, which is the dominant K
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Registered trials
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