Background: Microtia is a congenital outer ear deformity that causes the auricle to be absent or underdeveloped. It is frequently associated with external auditory canal atresia and causes hearing and psychosocial problems. Objectives: We thoroughly investigate the aspects of microtia and explore both current and innovative therapies. Methods: A systematic literature review was conducted following PRISMA guidelines, focusing on microtia and reconstruction methodologies. This review utilized three databases: PubMed, Scopus, and Web of Science. Results: The etiology involves both genetic and environmental factors and can occur as part of a syndrome or as an isolated condition. Clinically, it has esthetic and functional implications, potentially leading to conductive hearing loss. A multidisciplinary approach is essential for treatment, which includes surgical reconstruction using autologous cartilage or synthetic prostheses. Advances in bioengineering and 3D printing offer new, less invasive solutions. Conclusions: This review aims to synthesize current knowledge on microtia, focusing on tissue engineering for auricular reconstruction, identifying research gaps, evaluating techniques, and providing a resource for clinicians to improve decision-making and foster further research.

Hearing loss can result from impairments in structures that support endocochlear potential, as they play a crucial role in the transduction and transmission of auditory waves. This aspect has been the subject of several studies to date. In our review, the role of ion transport channels and pumps involved in hearing function has been highlighted, emphasizing how important the Kir4.1 channel is in maintaining the endocochlear potential. The Kir4.1 channel, a member of the inwardly rectifying potassium channel (Kir) family, plays a key role in the regulation of cell electrical activity and potassium ion homeostasis. The cochlear expression of these channels is at the level of the intermediate cells of the vascular stria, in the root cells of the outer sulcus, and in the glial cells of the spiral ganglion. In development, its expression demonstrates its involvement in the progression of pathologies related to potassium channel dysfunction, and its activation in the stria vascularis is directly related to the generation of endocochlear potential. Kir4.1 is fundamental in stabilizing the resting membrane potential of cells and modulating their excitability, as it facilitates a greater influx of potassium into cells compared to efflux when the membrane potential is negative. Mutations in the K⁺ channel gene KCNJ10 (Kir4.1) have been associated with several disorders, with the most significant studies on EAST/SeSAME syndrome and Pendred syndrome. Recent research has explored the metabolic importance of potassium channel changes associated with stria vascularis degeneration in the progression of age-related hearing loss. Furthermore, in ototoxicity studies, the Kir4.1 channel has been shown to have the ability to compensate for the deficiency of other K⁺ channels, as it maintains the cochlear homeostasis by correcting the imbalanced K⁺ concentration.

Cisplatin (cis-diclorodiamminoplatin, CDDP) is a common chemotherapeutic agent for solid tumors, but its use is limited by severe side effects such as ototoxicity and nephrotoxicity. Variability in CDDP dosing and administration, along with high mortality and sensitivity in animal models, complicates experimental approaches. This study aimed to evaluate ototoxic damage in rats by comparing a single bolus versus three divided CDDP injections, also considering nephrotoxic effects. Twenty-four Sprague-Dawley rats were divided into three groups: eight received a single intraperitoneal injection of CDDP (14 mg/kg), eight received three injections (4.6 mg/kg/day), and eight were untreated controls. All CDDP-treated rats showed significant high-frequency hearing loss and morphological damage, including cochlear outer hair cell loss and renal glomerular atrophy with proximal tubule necrosis. Oxidative stress markers (nitrotyrosine and SOD1 expression) confirmed cochlear and renal alterations. Notably, the single bolus group had a 25% mortality rate and significant weight loss among survivors, unlike the other groups. This study introduces the novel finding that cumulative administration of three doses reduces mortality and weight loss while maintaining similar ototoxic and nephrotoxic effects. Therefore, cumulative administration is recommended for future studies to mitigate ototoxic and nephrotoxic damage, offering a potentially improved protocol for the administration of cisplatin.