MALAT1 as a Diagnostic and Therapeutic Target in Diabetes-Related Complications: A Promising Long-Noncoding RNA

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Abstract

Diabetes mellitus is a global issue with increasing incidence rate worldwide. In an uncontrolled case, it can advance to various organ-related complications leading to an increase in morbidity and mortality. Long non-coding RNA (lncRNA) Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) appears to be a fairly novel lncRNA that is relevant to diabetes and its role in diabetic-related diseases initiation and progression have long been a subject of attention to many scholars. The expression of MALAT1 is elevated in different diabetic-related diseases. In this review, we demonstrate the various functions of MALAT1 in the different diabetes-related complications including ischemic reperfusion injury, retinopathy, cataract, atherosclerosis, cardiomyopathy, non-alcoholic steatohepatitis, gastroparesis, kidney disease, and gestational diabetes. The emerging evidence showed that the role of MALAT1 in diabetic-related complications is both pro-inflammatory and apoptosis in different cell types. These results concluded that MALAT1 is a potential diagnostic and future targeted therapy for diabetes-associated complications.

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Most cited references 46

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Inflammation: the link between insulin resistance, obesity and diabetes.

Paresh Dandona, Ahmad Aljada, Arindam Bandyopadhyay (2004)

Recent data have revealed that the plasma concentration of inflammatory mediators, such as tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), is increased in the insulin resistant states of obesity and type 2 diabetes, raising questions about the mechanisms underlying inflammation in these two conditions. It is also intriguing that an increase in inflammatory mediators or indices predicts the future development of obesity and diabetes. Two mechanisms might be involved in the pathogenesis of inflammation. Firstly, glucose and macronutrient intake causes oxidative stress and inflammatory changes. Chronic overnutrition (obesity) might thus be a proinflammatory state with oxidative stress. Secondly, the increased concentrations of TNF-alpha and IL-6, associated with obesity and type 2 diabetes, might interfere with insulin action by suppressing insulin signal transduction. This might interfere with the anti-inflammatory effect of insulin, which in turn might promote inflammation.

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A glimpse of various pathogenetic mechanisms of diabetic nephropathy.

Yashpal S Kanwar, Lin Sun, Ping Xie … (2011)

Diabetic nephropathy is a well-known complication of diabetes and is a leading cause of chronic renal failure in the Western world. It is characterized by the accumulation of extracellular matrix in the glomerular and tubulointerstitial compartments and by the thickening and hyalinization of intrarenal vasculature. The various cellular events and signaling pathways activated during diabetic nephropathy may be similar in different cell types. Such cellular events include excessive channeling of glucose intermediaries into various metabolic pathways with generation of advanced glycation products, activation of protein kinase C, increased expression of transforming growth factor β and GTP-binding proteins, and generation of reactive oxygen species. In addition to these metabolic and biochemical derangements, changes in the intraglomerular hemodynamics, modulated in part by local activation of the renin-angiotensin system, compound the hyperglycemia-induced injury. Events involving various intersecting pathways occur in most cell types of the kidney.

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Pathogenic role of lncRNA-MALAT1 in endothelial cell dysfunction in diabetes mellitus

J. Liu, J J A Yao, X. M. Li … (2014)

Long noncoding RNAs (lncRNAs) have important roles in diverse biological processes. Our previous study has revealed that lncRNA-MALAT1 deregulation is implicated in the pathogenesis of diabetes-related microvascular disease, diabetic retinopathy (DR). However, the role of MALAT1 in retinal vasculature remodeling still remains elusive. Here we show that MALAT1 expression is significantly upregulated in the retinas of STZ-induced diabetic rats and db/db mice. MALAT1 knockdown could obviously ameliorate DR in vivo, as shown by pericyte loss, capillary degeneration, microvascular leakage, and retinal inflammation. Moreover, MALAT1 knockdown could regulate retinal endothelial cell proliferation, migration, and tube formation in vitro. The crosstalk between MALAT1 and p38 MAPK signaling pathway is involved in the regulation of endothelial cell function. MALAT1 upregulation represents a critical pathogenic mechanism for diabetes-induced microvascular dysfunction. Inhibition of MALAT1 may serve as a potential target for anti-angiogenic therapy for diabetes-related microvascular complications.

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Author and article information

Journal

Journal ID (nlm-ta): Int J Med Sci

Journal ID (iso-abbrev): Int J Med Sci

Journal ID (publisher-id): ijms

Title: International Journal of Medical Sciences

Publisher: Ivyspring International Publisher (Sydney )

ISSN (Electronic): 1449-1907

Publication date Collection: 2019

Publication date (Electronic): 20 April 2019

Volume: 16

Issue: 4

Pages: 548-555

Affiliations

[1 ]Department of Ophthalmology,

[2 ]Department of Radiology,

[3 ]Department of Endocrinology, The First Hospital of Jilin University, No. 71 of Xinmin St. Changchun, Jilin Province, 130021, China.

Author notes

✉ Corresponding author: Cheng-wei Lu, M.D., Ph.D., Department of Ophthalmology, the First Hospital of Jilin University, No. 71 of Xinmin St. Changchun, Jilin Province, 130021, China. Email address: lcwchina800@ 123456sina.com ; Telephone No: +8618684317115.

* Leila Elmi Abdulle, Ji-long Hao, Om Prakash Pant, Xiu-fen Liu, Dan-Dan Zhou, Ying Gao and Abhishek Suwal are co-first authors.

Competing Interests: The authors have declared that no competing interest exists.

Article

Publisher ID: ijmsv16p0548

DOI: 10.7150/ijms.30097

PMC ID: 6535662

PubMed ID: 31171906

SO-VID: 8eb38059-82d0-493e-a8fd-06ae1b26fa8c

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This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license ( https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.

MALAT1 as a Diagnostic and Therapeutic Target in Diabetes-Related Complications: A Promising Long-Noncoding RNA

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International Journal of Applied Technology in Medical Sciences

Most cited references 46

Inflammation: the link between insulin resistance, obesity and diabetes.

A glimpse of various pathogenetic mechanisms of diabetic nephropathy.

Pathogenic role of lncRNA-MALAT1 in endothelial cell dysfunction in diabetes mellitus

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