Abstract
Due to the lack of an effective method for the treatment of fibrosis, there are numerous patients suffering from the effects of fibrosis. Severe fibrosis can cause dysfunction of relevant organs characterized by excessive deposition of extracellular matrix components. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA that is widely expressed and highly conserved in human tissues. It can regulate gene expression at various molecular levels, involved in the fibrosis of the liver, heart, lung, and kidney. In this review, we first described the pathogenesis by which MALAT1 promotes fibrosis. Furthermore, we summarized current studies of MALAT1 in the fibrosis of various organs. Hope this review will contribute to a better understanding of the molecular mechanism of fibrosis and the potential of MALAT1 as a novel therapeutic target for fibrosis.
Highlights
Fibrosis is a complex biological process characterized by abnormal inflammatory damage and excessive accumulation of the extracellular matrix (ECM) [1], which may involve a variety of tissues and organs, such as the heart, liver, kidney and lung [2,3,4,5]
The results revealed that Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) acts as a competitive endogenous RNA of miR-101b to influence hepatic stellate cells (HSCs) activation, proliferation, and the cell cycle by regulating related C3 botulinum toxin substrate1 (Rac1) expression, which leads to liver fibrosis [72]
Whole-genome expression analysis and small ribonucleic acid sequencing revealed only minor differences between the two groups. The reason for this phenomenon may be due to the fact that during the mouse embryonic development stage, the researchers knocked out the MALAT1 gene, thereby activating other compensatory mechanisms in the body to cover up the effect of the knockout of the MALAT1 gene, or the role of MALAT1 is limited in related signal pathways in vivo
Summary
Fibrosis is a complex biological process characterized by abnormal inflammatory damage and excessive accumulation of the extracellular matrix (ECM) [1], which may involve a variety of tissues and organs, such as the heart, liver, kidney and lung [2,3,4,5]. Connective tissue deposition is a physiological phenomenon [8], excessive or progressive fibrosis leads to the destruction of tissue structure, resulting in organ dysfunction and even organ failure [9,10,11,12]. The number of people affected by fibrosis-related diseases has reached nearly 1/4 of the total global population [16], resulting in a heavy burden and tremendous challenge for the global medical system. Most treatment methods are still in the preclinical evaluation stage, and systemic inhibition of fibrosis-related signals will inevitably produce serious adverse reactions. IImmmmuunnee cceellllss rreelleeaassee ccyyttookkiinneess,, ssuucchhaass ttrraannssffoorrmmiinnggggrroowwtthhffaaccttoorr--ββ ((TTGGFF--ββ)),, aanndd ffiibbrroobbllaassttss pprroolliiffeerraatteeaannddttrraannssddiiff-ffeerreennttiiaattee iinnttoommyyoofifbibrorobblalsatsst,sl,elaedaidnigngtoteoxterxatcrealcluelllaurlmaramtriaxtr(iExC(MEC) dMe)pdoseiptioosnit.iMone.taMsteatsaisst-aassisso-caisastoecdialutendg laudnegnoacdaerncio-cnaormciantroamnsacrtripant s1c(rMipAt 1LA(MT1A)LpAlaTy1s)dpilfafeyrsednitfrfeorlesntinrorleegsuilnatriengguelatcihngofetahcehaobfotvhe lainbokvs.e links
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