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Back to the Origin: Mechanisms of circRNA-Directed Regulation of Host Genes in Human Disease.
Noncoding RNA
September 2024
Center of Forensic Investigation, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, China.
Circular RNAs (circRNAs) have been shown to be pivotal regulators in various human diseases by participating in gene splicing, acting as microRNA (miRNA) sponges, interacting with RNA-binding proteins (RBPs), and translating into short peptides. As the back-splicing products of pre-mRNAs, many circRNAs can modulate the expression of their host genes through transcriptional, post-transcriptional, translational, and post-translational control via interaction with other molecules. This review provides a detailed summary of these regulatory mechanisms based on the class of molecules that they interact with, which encompass DNA, mRNA, miRNA, and RBPs.
View Article and Find Full Text PDFANGPTL4 May Regulate the Crosstalk Between Intervertebral Disc Degeneration and Type 2 Diabetes Mellitus: A Combined Analysis of Bioinformatics and Rat Models.
J Inflamm Res
December 2023
Shanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedic Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, People's Republic of China.
Introduction: The crosstalk between intervertebral disc degeneration (IVDD) and type 2 diabetes mellitus (T2DM) has been investigated. However, the common mechanism underlying this phenomenon has not been clearly elucidated. This study aimed to explore the shared gene signatures of IVDD and T2DM.
View Article and Find Full Text PDFCell-cell communication in kidney fibrosis.
Nephrol Dial Transplant
April 2024
State Key Laboratory of Organ Failure Research, Division of Nephrology, Nanfang Hospital, Southern Medical University.
Kidney fibrosis is a common outcome of a wide variety of chronic kidney diseases, in which virtually all kinds of renal resident and infiltrating cells are involved. As such, well-orchestrated intercellular communication is of vital importance in coordinating complex actions during renal fibrogenesis. Cell-cell communication in multicellular organisms is traditionally assumed to be mediated by direct cell contact or soluble factors, including growth factors, cytokines and chemokines, through autocrine, paracrine, endocrine and juxtacrine signaling mechanisms.
View Article and Find Full Text PDFRegulation of whole-transcriptome sequencing expression in COPD after personalized precise exercise training: a pilot study.
Respir Res
June 2023
Department of Pulmonary and Critical Care Medicine, Shanghai Pudong New Area Gongli Hospital, 219 MiaoPu Road, Shanghai, 200315, People's Republic of China.
Background: Chronic obstructive pulmonary disease (COPD) is one of the world's leading causes of death and a major chronic respiratory disease. Aerobic exercise, the cornerstone of pulmonary rehabilitation, improves prognosis of COPD patients; however, few studies have comprehensively examined the changes in RNA transcript levels and the crosstalk between various transcripts in this context. This study identified the expression of RNA transcripts in COPD patients who engaged in aerobic exercise training for 12 weeks, and further constructions of the possible RNAs networks were made.
View Article and Find Full Text PDFWhole-transcriptome sequencing identifies key differentially expressed circRNAs/lncRNAs/miRNAs/mRNAs and linked ceRNA networks in adult degenerative scoliosis.
Front Mol Neurosci
March 2023
The Second Affiliated Hospital of Kunming Medical University, Kunming Medical University, Kunming, China.
Background: Adult degenerative scoliosis (ADS) is forecast to be a prevalent disabling condition in an aging society. Universally, its pathogenesis is perceived as intervertebral disc degeneration (IDD), however, a thought-provoking issue is why precisely a subset of patients with disc degeneration develop ADS. Exploring the diversities between common IDD and ADS would contribute to unraveling the etiological mechanisms of ADS.
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