98%
921
2 minutes
20
The cochlear structure is highly complex and specific, and its development is regulated by multiple signaling pathways. Abnormalities in cochlear development can lead to different degrees of loss of function. Hair cells (HCs), which are difficult to regenerate in the mature mammalian cochlea, are susceptible to damage from noise and ototoxic drugs, and damage to HCs can cause hearing loss to varying degrees. Notch, a classical developmental signaling molecule, has been shown to be closely associated with embryonic cochlear development and plays an important role in HC regeneration in mammals, suggesting that the Notch signaling pathway may be a potential therapeutic target for cochlear development and hearing impairment due to HC damage. In recent years, the important role of the Notch signaling pathway in the cochlea has received increasing attention. In this paper, we review the role of Notch signaling in cochlear development and HC regeneration, with the aim of providing new research ideas for the prevention and treatment of related diseases.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.2174/0113816128273532231103110910 | DOI Listing |
Neuroendocrinology
September 2025
Introduction Neuroendocrine tumors (NETs) are a rare and heterogeneous group of neoplasms with both clinical and genetic diversity. The clinical applicability of molecular profiling using liquid biopsy for identifying actionable drug targets and prognostic indicators in patients with advanced NETs remains unclear. Methods In this study, we utilized a custom-made 37 genes panel of circulating tumor DNA (ctDNA) based on next-generation sequencing (NGS) in 47 patients with advanced NETs.
View Article and Find Full Text PDFMediators Inflamm
September 2025
College of Ophthalmology and Optometry, Shandong University of Traditional Chinese Medicine, Jinan 250002, China.
Uveitis is an inflammatory eye disease, and Longdan Xiegan Decoction (LXD) has been used to treat uveitis. However, the underlying mechanisms have not fully been addressed. The present study aimed to provide new insights into LXD ameliorating inflammatory response of experimental autoimmune uveitis (EAU) and regulating T helper (Th) cell differentiation via the interaction between microRNA (miRNA) and mRNA.
View Article and Find Full Text PDFKorean J Physiol Pharmacol
September 2025
Department of Physiology & Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Korea.
Diabetes mellitus is a major global health concern associated with micro-and macrovascular complications. Among the diverse mechanisms that contribute to vascular dysfunction in diabetes, endothelial to mesenchymal transition (EndMT) has emerged as a key pathological process. EndMT involves the loss of endothelial cell characteristics and the acquisition of mesenchymal features, resulting in impaired endothelial function, increased fibrosis, and inflammation.
View Article and Find Full Text PDFMed
August 2025
Joint Academic Rheumatology Program, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece; Centre of New Biotechnologies and Precision Medicine (CNBPM), School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece. Electronic address: p
Background: Pathogenic responses against self and foreign antigens in systemic autoimmunity and infection, respectively, engage similar immunologic components, thus lacking distinguishing diagnostic biomarkers. Herein, we tested whether whole-blood transcriptome analysis discriminates autoimmune from infectious diseases.
Methods: We applied nested cross-validation methodology to tune and validate random forests, k-nearest neighbors, and support vector machines, using a new preprocessing method on 22 publicly available datasets, including 594 patients with a broad spectrum of systemic autoimmune diseases and 615 patients with diverse viral, bacterial, and parasitic infections.
Exp Cell Res
September 2025
Organ Transplant Center, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510080, China; Guangdong Provincial Key Laboratory of Organ Donation and Transplant Immunology, Guangzhou, Guangdong 510080, China. Electronic address:
Background: Chronic rejection is a major cause of long-term kidney allograft failure, characterized by persistent inflammation and progressive fibrosis. Macrophages are central mediators of this process, but their phenotypic heterogeneity and regulatory mechanisms in chronic rejection remain incompletely understood.
Methods: We performed single-cell transcriptomic analysis on renal allograft biopsies from patients with different types of rejection and on a time-course rat model of chronic rejection.