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Site-Specific Lysine Lactylation via Genetic Code Expansion in E. coli and Mammalian Cells
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Lactylation Modification: From Basic Biological Process to Clinical Cardiovascular Diseases.

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This summary is machine-generated.

Lactate, once a waste product, is now known to regulate gene expression through lysine lactylation (Kla). This metabolic-epigenetic process impacts cardiovascular diseases, offering new therapeutic targets.

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Cardiovascular diseases (CVDs) are a leading cause of death, characterized by metabolic and tissue remodeling issues.
  • Lactate is recognized as a signaling metabolite and carbon source, not just waste.
  • Lysine lactylation (Kla) links lactate levels to protein function and chromatin state.

Purpose of the Study:

  • To synthesize current knowledge on lysine lactylation (Kla) in cardiovascular diseases.
  • To explore the role of Kla in regulating transcriptional and signaling networks.
  • To identify therapeutic strategies targeting the lactate-lactylation axis in CVDs.

Main Methods:

  • Review and synthesis of existing literature on lactate metabolism and protein lactylation.
  • Analysis of the enzymatic regulation and biogenesis of Kla.
  • Examination of Kla's role in various cardiovascular pathologies.

Main Results:

  • Lactate-driven lactylation influences fibrosis, metabolism, inflammation, and angiogenesis.
  • Kla acts as a key regulator in atherosclerosis, myocardial infarction, heart failure, and other CVDs.
  • Kla can either accelerate or inhibit disease progression depending on the context.

Conclusions:

  • Protein lactylation represents a critical metabolic-epigenetic interface in the cardiovascular system.
  • Targeting the lactate-lactylation axis offers potential for precision therapies in CVDs.
  • Further research into lactate transport, production, and lactylation modifiers is warranted.