Related Experiment Video
Updated: Sep 12, 2025
09:36
RNA Pull-down Procedure to Identify RNA Targets of a Long Non-coding RNA
Published on: April 10, 2018
25.5K
Long non-coding RNA MALAT1: A crucial factor in fibrotic diseases
Linbin Ran1, Wei Pan2, Jianguo Feng3
1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing 400044, China.
Molecular Therapy. Nucleic Acids
|August 8, 2025
Summary
Long non-coding RNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) is implicated in fibrotic diseases. This review explores MALAT1
Area of Science:
- Molecular Biology
- Genetics
- Pathophysiology
Background:
- Long non-coding RNAs (lncRNAs) are crucial regulators in biological processes and disease development.
- The lncRNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) is recognized for its roles in cell proliferation, apoptosis, and disease pathogenesis.
- Emerging evidence suggests a significant link between MALAT1 and the development and progression of fibrotic diseases.
Purpose of the Study:
- To review and synthesize current research on the association between MALAT1 and various fibrotic conditions.
- To elucidate the molecular mechanisms underlying the interaction of MALAT1 in hepatic, pulmonary, renal, and myocardial fibrosis.
- To identify and discuss MALAT1-targeted therapeutic strategies for fibrotic diseases.
Main Methods:
- Literature review of existing studies on MALAT1 and fibrotic diseases.
- Analysis of molecular pathways and mechanisms involving MALAT1 in fibrosis.
- Compilation of current MALAT1-targeting agents and therapeutic approaches.
Main Results:
- MALAT1 plays a significant role in the pathogenesis of multiple fibrotic diseases.
- Specific molecular mechanisms linking MALAT1 to fibrosis are identified across different organs.
- Various MALAT1-targeted agents, including nucleic acid drugs and small-molecule inhibitors, are available.
Conclusions:
- MALAT1 is a key player in the pathophysiology of diverse fibrotic diseases.
- Understanding MALAT1's molecular functions offers potential therapeutic targets for treating fibrosis.
- Targeting MALAT1 presents a promising strategy for the development of novel antifibrotic therapies.
More Related Videos
Related Concept Videos
02:39lncRNA - Long Non-coding RNAs
8.9K
In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...
8.9K
01:13Formation of Muscle Fibers from Myoblasts
5.1K
De novo myogenesis, or the formation of muscle fibers, begins during the early embryonic stages. The skeletal muscle is formed from somites– blocks of embryonic cell layers. The somites are further divided into dermatomes, myotomes, sclerotomes, and syndetomes. Among these, the myotomes give rise to muscle fibers.
Muscle progenitor cells (MPCs) are formed from the myotomes. MPCs express genes that encode the transcription factors Pax3 and Pax7. Along with Pax 3/7, other transcription...
Muscle progenitor cells (MPCs) are formed from the myotomes. MPCs express genes that encode the transcription factors Pax3 and Pax7. Along with Pax 3/7, other transcription...
5.1K
03:18Non-LTR Retrotransposons
11.9K
As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
11.9K