Non-Coding RNA, Fibrogenesis, and Fibrotic Disease

A special issue of Non-Coding RNA (ISSN 2311-553X).

Deadline for manuscript submissions: closed (31 January 2019) | Viewed by 22154

Special Issue Editor


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Guest Editor
Diabetes and Fibrotic Disease Research Unit, Translational Genomics Research Institute, 445 N 5th Street, Phoenix, AZ 85004, USA
Interests: ncRNA; epigenetics; nonalcoholic fatty liver disease; hepatic fibrosis; microvascular complications of type 2 diabetes; gene expression

Special Issue Information

Dear Colleagues,

Fibrosis describes the accumulation of extracellular matrix proteins in response to injury. Under pathological conditions, such as chronic inflammation, fibrosis results in scarring of the affected tissue and compromises normal organ function. Fibrosis affects a wide range of organs, resulting in diseases such as nonalcoholic steatohepatitis (NASH), idiopathic pulmonary fibrosis (IPF), cystic fibrosis, atrial fibrosis, and renal fibrosis. Accumulating evidence suggests that fibrosis may be reversible in some organs; however, the mechanisms underlying this process remain incompletely elucidated. In other organs, such as lung, fibrosis is not curable and the prognosis for IPF patients is dismal. Further, the clinical course of fibrotic disease is heterogeneous and methods for predicting disease trajectory are lacking. In some organs, fibrotic disease oftentimes manifests symptoms past the point where treatment strategies are effective, yet non-invasive methods for the accurate detection of fibrosis are not yet available in many tissues. Given the significant clinical impact of fibrotic disease, efforts to understand the development and progression of fibrosis across myriad tissues and organs represent an active area of research.

Recent work has shown a role for non-coding RNA (ncRNA) in the pathogenesis and progression of fibrotic disease. The potential of ncRNAs to serve as biomarkers and targets for drug development in fibrotic disease is also becoming more fully appreciated. For this Special Issue, we invite colleagues exploring the intersection between ncRNAs and fibrotic disease to submit original research, methods, and review manuscripts on the role and function of miRNAs, lncRNAs, and other ncRNAs in the development, regulation, and reversal of fibrosis, as well as the clinical utility of ncRNAs in the diagnosis, prognosis, or treatment of fibrotic diseases.

Prof. Johanna K. DiStefano
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Non-Coding RNA is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • ncRNA
  • miRNA
  • lncRNA
  • fibrosis
  • fibrotic disease
  • fibrogenesis
  • biomarker
  • hepatic fibrosis
  • cystic fibrosis
  • idiopathic pulmonary fibrosis
  • atrial fibrosis

Published Papers (4 papers)

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Review

25 pages, 1168 KiB  
Review
Increased Extracellular Matrix Protein Production in Chronic Diabetic Complications: Implications of Non-Coding RNAs
by Saumik Biswas and Subrata Chakrabarti
Non-Coding RNA 2019, 5(1), 30; https://doi.org/10.3390/ncrna5010030 - 22 Mar 2019
Cited by 20 | Viewed by 4735
Abstract
Management of chronic diabetic complications remains a major medical challenge worldwide. One of the characteristic features of all chronic diabetic complications is augmented production of extracellular matrix (ECM) proteins. Such ECM proteins are deposited in all tissues affected by chronic complications, ultimately causing [...] Read more.
Management of chronic diabetic complications remains a major medical challenge worldwide. One of the characteristic features of all chronic diabetic complications is augmented production of extracellular matrix (ECM) proteins. Such ECM proteins are deposited in all tissues affected by chronic complications, ultimately causing organ damage and dysfunction. A contributing factor to this pathogenetic process is glucose-induced endothelial damage, which involves phenotypic transformation of endothelial cells (ECs). This phenotypic transition of ECs, from a quiescent state to an activated dysfunctional state, can be mediated through alterations in the synthesis of cellular proteins. In this review, we discussed the roles of non-coding RNAs, specifically microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), in such processes. We further outlined other epigenetic mechanisms regulating the biogenesis and/or function of non-coding RNAs. Overall, we believe that better understanding of such molecular processes may lead to the development of novel biomarkers and therapeutic strategies in the future. Full article
(This article belongs to the Special Issue Non-Coding RNA, Fibrogenesis, and Fibrotic Disease)
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13 pages, 2043 KiB  
Review
Biogenesis, Stabilization, and Transport of microRNAs in Kidney Health and Disease
by Melissa J. Thomas, Donald J. Fraser and Timothy Bowen
Non-Coding RNA 2018, 4(4), 30; https://doi.org/10.3390/ncrna4040030 - 03 Nov 2018
Cited by 9 | Viewed by 4963
Abstract
The kidneys play key roles in the maintenance of homeostasis, including fluid balance, blood filtration, erythropoiesis and hormone production. Disease-driven perturbation of renal function therefore has profound pathological effects, and chronic kidney disease is a leading cause of morbidity and mortality worldwide. Successive [...] Read more.
The kidneys play key roles in the maintenance of homeostasis, including fluid balance, blood filtration, erythropoiesis and hormone production. Disease-driven perturbation of renal function therefore has profound pathological effects, and chronic kidney disease is a leading cause of morbidity and mortality worldwide. Successive annual increases in global chronic kidney disease patient numbers in part reflect upward trends for predisposing factors, including diabetes, obesity, hypertension, cardiovascular disease and population age. Each kidney typically possesses more than one million functional units called nephrons, and each nephron is divided into several discrete domains with distinct cellular and functional characteristics. A number of recent analyses have suggested that signaling between these nephron regions may be mediated by microRNAs. For this to be the case, several conditions must be fulfilled: (i) microRNAs must be released by upstream cells into the ultrafiltrate; (ii) these microRNAs must be packaged protectively to reach downstream cells intact; (iii) these packaged microRNAs must be taken up by downstream recipient cells without functional inhibition. This review will examine the evidence for each of these hypotheses and discuss the possibility that this signaling process might mediate pathological effects. Full article
(This article belongs to the Special Issue Non-Coding RNA, Fibrogenesis, and Fibrotic Disease)
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12 pages, 733 KiB  
Review
LncRNAs in TGF-β-Driven Tissue Fibrosis
by Patrick Ming-Kuen Tang, Ying-Ying Zhang and Hui-Yao Lan
Non-Coding RNA 2018, 4(4), 26; https://doi.org/10.3390/ncrna4040026 - 04 Oct 2018
Cited by 31 | Viewed by 4846
Abstract
Transforming growth factor-β (TGF-β) is a crucial mediator in tissue fibrosis that promotes accumulation of extracellular matrix (ECM), myofibroblasts to epithelial–mesenchymal transition (EMT), endothelial-mesenchymal transition (EndoMT), and apoptosis via canonical and noncanonical signaling pathways. In the past decades, a number of microRNAs have [...] Read more.
Transforming growth factor-β (TGF-β) is a crucial mediator in tissue fibrosis that promotes accumulation of extracellular matrix (ECM), myofibroblasts to epithelial–mesenchymal transition (EMT), endothelial-mesenchymal transition (EndoMT), and apoptosis via canonical and noncanonical signaling pathways. In the past decades, a number of microRNAs have been reported to participate in TGF-β-mediated tissue scarring; however, the roles of long noncoding RNAs (lncRNAs) in fibrogenesis remain largely unknown. Recently, emerging evidence has shown that lncRNAs are involved in the development of different diseases, including cancer, autoimmune diseases, cardiovascular diseases, and fibrotic diseases. In this review, we summarize the current updates of lncRNAs in TGF-β1-driven tissue fibrosis and discuss their therapeutic potential for the treatment of chronic fibrotic diseases. Full article
(This article belongs to the Special Issue Non-Coding RNA, Fibrogenesis, and Fibrotic Disease)
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15 pages, 465 KiB  
Review
The Role of Long Non-Coding RNAs (lncRNAs) in the Development and Progression of Fibrosis Associated with Nonalcoholic Fatty Liver Disease (NAFLD)
by Amanda Hanson, Danielle Wilhelmsen and Johanna K. DiStefano
Non-Coding RNA 2018, 4(3), 18; https://doi.org/10.3390/ncrna4030018 - 21 Aug 2018
Cited by 44 | Viewed by 7065
Abstract
Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of conditions ranging from hepatic steatosis to inflammation (nonalcoholic steatohepatitis or NASH) with or without fibrosis, in the absence of significant alcohol consumption. The presence of fibrosis in NASH patients is associated with greater liver-related [...] Read more.
Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of conditions ranging from hepatic steatosis to inflammation (nonalcoholic steatohepatitis or NASH) with or without fibrosis, in the absence of significant alcohol consumption. The presence of fibrosis in NASH patients is associated with greater liver-related morbidity and mortality; however, the molecular mechanisms underlying the development of fibrosis and cirrhosis in NAFLD patients remain poorly understood. Long non-coding RNAs (lncRNAs) are emerging as key contributors to biological processes that are underpinning the initiation and progression of NAFLD fibrosis. This review summarizes the experimental findings that have been obtained to date in animal models of liver fibrosis and NAFLD patients with fibrosis. We also discuss the potential applicability of circulating lncRNAs to serve as biomarkers for the diagnosis and prognosis of NAFLD fibrosis. A better understanding of the role played by lncRNAs in NAFLD fibrosis is critical for the identification of novel therapeutic targets for drug development and improved, noninvasive methods for disease diagnosis. Full article
(This article belongs to the Special Issue Non-Coding RNA, Fibrogenesis, and Fibrotic Disease)
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