MicroRNAs and Regulation of Autophagy in Chondrocytes
Methods in Molecular Biology, ISSN: 1940-6029, Vol: 2245, Page: 179-194
2021
- 4Citations
- 8Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations4
- Citation Indexes4
- Captures8
- Readers8
Book Chapter Description
Chondrocytes are the main cells responsible for the maintenance of cartilage homeostasis and integrity. During development, extracellular matrix (ECM) macromolecules are produced and deposited by chondrocyte precursors. Autophagy, a highly dynamic process aimed at degradation of dysfunctional or pathogenic proteins, organelles, and intracellular microbes that can damage tissues, is one of the key processes required for sustained cartilage homeostasis. In different cell types it has been shown that, among others, autophagy is regulated by epigenetic mechanisms such as small noncoding RNAs (miRNAs, ~22 base pairs). Increasing evidence suggests that miRNAs are also involved in the regulation of autophagy in chondrocytes. Based on our previous research of gene and miRNA expression in articular cartilage, in this chapter we provide a summary of the tools models to direct in vitro and in vivo studies aimed at gaining a better understanding of the regulatory roles of miRNAs in chondrocyte autophagy.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85097882620&origin=inward; http://dx.doi.org/10.1007/978-1-0716-1119-7_13; http://www.ncbi.nlm.nih.gov/pubmed/33315203; https://link.springer.com/10.1007/978-1-0716-1119-7_13; https://dx.doi.org/10.1007/978-1-0716-1119-7_13; https://link.springer.com/protocol/10.1007/978-1-0716-1119-7_13
Springer Science and Business Media LLC
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