AI Article Synopsis
- Lactylation (Kla) is a newly found chemical modification that comes from lactate and is important for many cell functions, but its role in hypertrophic scar formation isn't well understood.
- Researchers identified 1023 lactylation sites from 338 nonhistone proteins in hypertrophic scars and normal skin, as well as 2008 proteins overall in these tissues.
- The study found that lactylation mainly affects genes related to ribosome function and glycolysis, with 14 specific lactylation sites significantly increased in hypertrophic scars, suggesting that lactylation could help regulate processes connected to scar formation.
Article Abstract
Lactylation (Kla), a recently discovered post-translational modification derived from lactate, plays crucial roles in various cellular processes. However, the specific influence of lactylation on the biological processes underlying hypertrophic scar formation remains unclear. In this study, we present a comprehensive profiling of the lactylome and proteome in both hypertrophic scars and adjacent normal skin tissues. A total of 1023 Kla sites originating from 338 nonhistone proteins were identified based on lactylome analysis. Proteome analysis in hypertrophic scar and adjacent skin samples revealed the identification of 2008 proteins. It is worth noting that Kla exhibits a preference for genes associated with ribosome function as well as glycolysis/gluconeogenesis in both normal skin and hypertrophic scar tissues. Furthermore, the functional enrichment analysis demonstrated that differentially lactyled proteins are primarily involved in proteoglycans, HIF-1, and AMPK signaling pathways. The combined analysis of the lactylome and proteome data highlighted a significant upregulation of 14 lactylation sites in hypertrophic scar tissues. Overall, our investigation unveiled the significant involvement of protein lactylation in the regulation of ribosome function as well as glycolysis/gluconeogenesis, potentially contributing to the formation of hypertrophic scars.
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| http://dx.doi.org/10.1021/acs.jproteome.3c00901 | DOI Listing |
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