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m6A control programmed cell death in cardiac fibrosis. | LitMetric

m6A control programmed cell death in cardiac fibrosis.

Life Sci

Department of Anesthesiology and Perioperative Medicine, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, PR China; Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, PR China. Electronic address:

Published: September 2024

AI Article Synopsis

  • * The regulation of m6A involves "writers" (methylases), "readers" (RNA-binding proteins), and "erasers" (demethylases), which work together to modify RNA dynamically.
  • * Recent research highlights the connection between m6A modification and programmed cell death (PCD), particularly focusing on how it affects four common types (apoptosis, autophagy, pyroptosis, and ferroptosis) in relation to cardiac fibrosis.

Article Abstract

N6-methyladenosine (m6A) modification is closely related to cardiac fibrosis. As the most common and abundant form of mRNA modification in eukaryotes, m6A is deposited by methylases ("writers"), recognized and effected by RNA-binding proteins ("readers"), and removed by demethylases ("erasers"), achieving highly dynamic reversibility. m6A modification is involved in regulating the entire biological process of target RNA, including transcription, processing and splicing, export from the nucleus to the cytoplasm, and enhancement or reduction of stability and translation. Programmed cell death (PCD) comprises many forms and pathways, with apoptosis and autophagy being the most common. Other forms include pyroptosis, ferroptosis, necroptosis, mitochondrial permeability transition (MPT)-dependent necrosis, and parthanatos. In recent years, increasing evidence suggests that m6A modification can mediate PCD, affecting cardiac fibrosis. Since the correlation between some PCD types and m6A modification is not yet clear, this article mainly introduces the relationship between four common PCD types (apoptosis, autophagy, pyroptosis, and ferroptosis) and m6A modification, as well as their role and influence in cardiac fibrosis.

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Source
http://dx.doi.org/10.1016/j.lfs.2024.122922DOI Listing

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