Abstract
Sensorineural hearing loss is a common sensory impairment in humans caused by abnormalities in the inner ear. The stria vascularis is regarded as a major cochlear structure that can independently degenerate and influence the degree of hearing loss. This review summarizes the current literature on the role of the stria vascularis in the pathogenesis of sensorineural hearing loss resulting from different etiologies, focusing on both molecular events and signaling pathways, and further attempts to explore the underlying mechanisms at the cellular and molecular biological levels. In addition, the deficiencies and limitations of this field are discussed. With the rapid progress in scientific technology, new opportunities are arising to fully understand the role of the stria vascularis in the pathogenesis of sensorineural hearing loss, which, in the future, will hopefully lead to the prevention, early diagnosis, and improved treatment of sensorineural hearing loss.
Highlights
Hearing loss is the most common sensory deficit in humans and has a negative influence on 430 million people worldwide, including 34 million children (World Health Organisation, 2021)
Previous studies have found that Na, K-ATPase, Na-K2Cl-Cotransporter (NKCC), Cl- channels CLCNKA/BSND, and CLCNKB/BSND are located in the basolateral membrane of marginal cells (Lang et al, 2007; Nin et al, 2016), the K + channel KCNQ1/KCNE1 is present in the apical membranes of marginal cells (Hibino et al, 2010), and the inwardly rectifying potassium channels Kir4.1 are expressed in the apical membranes of intermediate cells (Chen and Zhao, 2014)
In a guinea pig aging model, Zhou et al (2019) found that the expression of mRNA and protein levels of transmembrane protein 16 (TMEM16A), a calcium-activated chloride channel (CaCC), in the cochlear stria vascularis (SV) decreased, while the auditory brainstem response (ABR) thresholds increased. These findings suggest that the downregulation of TMEM16A may be related to ARHL and provide a potential new direction for clinical prevention and treatment of age-related hearing loss (Zhou et al, 2019)
Summary
Hearing loss is the most common sensory deficit in humans and has a negative influence on 430 million people worldwide, including 34 million children (World Health Organisation, 2021). Previous studies have found that Na, K-ATPase, Na-K2Cl-Cotransporter (NKCC), Cl- channels CLCNKA/BSND, and CLCNKB/BSND are located in the basolateral membrane of marginal cells (Lang et al, 2007; Nin et al, 2016), the K + channel KCNQ1/KCNE1 is present in the apical membranes of marginal cells (Hibino et al, 2010), and the inwardly rectifying potassium channels Kir4.1 are expressed in the apical membranes of intermediate cells (Chen and Zhao, 2014) These transporters and ion channels have been shown to be involved in the formation of EP, and inhibition of either transporter or ion channels could reduce EP (Nin et al, 2008). H(+) -ATPase (ATP6V1B1 and ATPV0A4) and bicarbonate/chloride transporter SLC26A4 (Pendrin) are expressed in the SV, and regulate the secretion of H+ and HCO3− in the endolymph to maintain pH homeostasis (Mittal et al, 2017); the Ca(2+) -ATPase and Ca(2+) channels expressed in the SV jointly maintain Ca(2+) homeostasis in the endolymph (Nin et al, 2016)
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