ArticlePeerJ2022
PIN1 protects auditory hair cells from senescence via autophagy.
Article in PeerJ, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed.
- Autophagy in Sensorineural Hearing Loss: Jekyll or Hyde?International journal of molecular sciences · 2026Review
- Review
- PIN1‑silencing mitigates keratinocyte proliferation and the inflammatory response in psoriasis by activating mitochondrial autophagy.Experimental and therapeutic medicine · 2024Article
- The molecular mechanisms of peptidyl-prolylFrontiers in pharmacology · 2024Review
- The Relevance of Autophagy within Inner Ear in Baseline Conditions and Tinnitus-Related Syndromes.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Age-related hearing loss is an increasing sensorineural hearing loss. But the pathogenesis of ARHL has not been clarified. Herein, we studied the role and significance of PIN1 in regulating autophagy activity in senescence HEI-OC1cells and HCs. Methods and Results: C57BL/6 mice and HEI-OC1 cells were contained in our research. Transfection of plasmids and juglone were used to upregulate or inhibit the PIN 1 expression. Immunofluorescence and Western blot were used to detect the expression of PIN1, LC3, p62, p21 and p16 protein levels in the hair cells of C57BL/6 mice cochleae and HEI-OC1 cells. Senescence-associated Conclusion: PIN1 might regulate autophagy activity to induce the senescent of HEI-OC1cells and HCs, which will provide a theoretical support for the prevention and treatment of age-related hearing loss.
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Registered trials
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