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Article

Ribosomal protein L13a deficiency in macrophages promotes atherosclerosis by limiting translation control-dependent retardation of inflammation.

Arteriosclerosis, thrombosis, and vascular biology - 1 Mar 2014

Basu Abhijit, Poddar Darshana, Robinet Peggy, Smith Jonathan D, Febbraio Maria, Baldwin William M, Mazumder Barsanjit

Abstract excerpt

OBJECTIVE: Unresolved inflammatory response of macrophages plays a pivotal role in the pathogenesis of atherosclerosis. Previously we showed that ribosomal protein L13a-dependent translational silencing suppresses the synthesis of a cohort of inflammatory proteins in monocytes and macrophages. We also found that genetic abrogation of L13a expression in macrophages significantly compromised the resolution of...

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Identifiers

PMID: 24436370
DOI: 10.1161/ATVBAHA.113.302573
PMCID: PMC3954853

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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