LncRNA: Shedding light on mechanisms and opportunities in fibrosis and aging

Yang, Zhi; Jiang, Shuai; Shang, Jiajia; Jiang, Yuting; Dai, Yu Cheng; Xu, Bin; Yu, Yuan; Liang, Zhenxing; Yang, Yang

doi:10.1016/j.arr.2019.04.001

Cited by 158 publications

(104 citation statements)

References 138 publications

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“…This finding suggests that the occurrence and development of hydrocephalus may be related to the differential expression of noncoding RNAs. At the same time, lncRNAs have been identified to have both promotive and inhibitory effects in the processes of fibrosis [37]. Liu et al [38] discovered that cholangiocyte-derived exoso-mallncRNAH19 can promote cholestatic liver fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Decreased MiR-30a promotes TGF-β1-mediated arachnoid fibrosis in post-hemorrhagic hydrocephalus

Zhan

Xiao

Zhang

et al. 2020

Translational Neuroscience

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AbstractBackgroundFibrosis in the ventricular system is closely associated with post-hemorrhagic hydrocephalus (PHH). It is characterized by an expansion of the cerebral ventricles due to CSF accumulation following intraventricular hemorrhage (IVH). The activation of transforming growth factor-β1 (TGF-β1) may be involved in thrombin-induced arachnoid fibrosis.MethodsA rat model of PHH was established by injection of autologous non-anticoagulated blood from the right femoral artery into the lateral ventricles. Differential expression of miR-30a was detected in rat arachnoid cells by RNA sequencing. AP-1, c-Fos, and TRAF3IP2 were knocked down in primary arachnoid cells, and the degree of arachnoid fibrosis was assessed.ResultsDecreased expression of miR-30a and increased expression of TRAF3IP2, TGF-β1, and α-SMA were detected in the arachnoid cells of PHH rat. Besides, overexpression of miR-30a targets TRAF3IP2 mRNA 3′UTR and inhibits the expression of TRAF3IP2, TGF-β1, and α-SMA in the primary arachnoid cells. Furthermore, TRAF3IP2 activates AP-1 to promote arachnoid fibrosis. The content of type I collagen in the primary arachnoid cells was reduced after the silencing of AP-1 and TRAF3IP2.ConclusionsThis study identified a miR-30a-regulated mechanism of arachnoid fibrosis, suggesting a previously unrecognized contribution of miR-30a to the pathogenesis of fibrosis in the ventricular system. These results might provide a new target for the clinical diagnosis and treatment of PHH.

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Section: Discussionmentioning

confidence: 99%

Decreased MiR-30a promotes TGF-β1-mediated arachnoid fibrosis in post-hemorrhagic hydrocephalus

Zhan

Xiao

Zhang

et al. 2020

Translational Neuroscience

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“…87 Some studies have suggested that age-related fibrosis may be due to decreased matrix degradation rather than increased collagen synthesis. 88,89 Macrophages secrete stromal cell proteins and are directly involved in ECM remodelling by producing MMPs and their inhibitors.…”

Section: With Ageing Turnover Of Crm Composition Contributes To Augmmentioning

confidence: 99%

Resident macrophages as potential therapeutic targets for cardiac ageing and injury

et al. 2020

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Cardiac‐resident macrophages (CRMs) play critical roles in maintaining cardiac homoeostasis and removing senescent and dying cells. Recent preclinical data have re‐energised the area of cardioimmunology and provided improved understanding of the modulation of compositional and functional phenotypes of CRMs. These data can aid in achieving improved cardiac regeneration, repair and functional remodelling following cardiac injury. In this review, we discuss the composition and renewal of various subsets of CRMs. Specific attention has been given to delineate the roles of various CRM subsets with respect to (1) facilitation of cardiac development and maintenance of physiological function such as electrical conduction and rhythm; (2) promotion of cardiac regeneration, inflammation resolution and functional remodelling following a cardiac injury; and (3) therapeutic potential. We have also highlighted the relationship between CRM replenishment and cardiomyocyte senescence as well as cardiovascular diseases development. Finally, we have addressed future perspectives and directions in basic research and potentially clinical applications of CRMs.

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“…Cardiac remodeling subsequently leads to the development of cardiac hypertrophy and fibrosis, an effect that is pronounced in aged hearts, leading to impairment of cardiac function [43]. Development of fibrosis has been considered to be the starting point of several pathophysiologies, which is initiated by an aberrant inflammatory response, and results in structural and functional deterioration of many organs [44].…”

Section: Aging and Cardiovascular Diseases And Epigeneticsmentioning

confidence: 99%

Epigenetics of aging and disease: a brief overview

et al. 2019

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Aging is an important risk factor for several human diseases such as cancer, cardiovascular disease and neurodegenerative disorders, resulting from a combination of genetic and environmental factors (e.g., diet, smoking, obesity and stress), which, at molecular level, cause changes in gene expression underlying the decline of physiological function. Epigenetics, which include mechanisms regulating gene expression independently of changes to DNA sequence, regulate gene expression by modulating the structure of chromatin or by regulating the binding of transcriptional machinery to DNA. Several studies showed that an impairment of epigenetic mechanisms promotes alteration of gene expression underlying several aging-related diseases. Alteration of these mechanisms is also linked with changes of gene expression that occurs during aging processes of different tissues. In this review, we will outline the potential role of epigenetics in the onset of two age-related pathologies, cancer and cardiovascular diseases.

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LncRNA: Shedding light on mechanisms and opportunities in fibrosis and aging

Cited by 158 publications

References 138 publications

Decreased MiR-30a promotes TGF-β1-mediated arachnoid fibrosis in post-hemorrhagic hydrocephalus

Decreased MiR-30a promotes TGF-β1-mediated arachnoid fibrosis in post-hemorrhagic hydrocephalus

Resident macrophages as potential therapeutic targets for cardiac ageing and injury

Epigenetics of aging and disease: a brief overview

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