Rpl3l, ribosomal protein L3-like, is a paralog of RPL3 specifically expressed in heart and skeletal muscle. It is involved in ribosome-related functions, influencing translation elongation dynamics, which is crucial for normal cardiac function [1]. It may also be associated with pathways like those related to cardiac muscle contraction and dilated cardiomyopathy [1]. Mouse models are valuable for studying its function.

In Rpl3l knockout male mice, the deficiency of RPL3L-containing ribosomes led to impaired cardiac contractility and altered ribosome occupancy at mRNA codons [1].

Rpl3l gene-deleted mice showed no overt cardiac changes at baseline or after pressure overload hypertrophy, likely due to up-regulation of RPL3, but by 18 months, they had significantly smaller hearts [2].

Rpl3l knockout mice also demonstrated increased ribosome-mitochondria interactions in cardiomyocytes and higher ATP levels, suggesting modulation of mitochondrial activity [3].

In conclusion, Rpl3l is essential for normal cardiac function through its impact on translation elongation dynamics and mitochondrial activity. Mouse knockout models have been instrumental in revealing its role in cardiac-related diseases such as dilated cardiomyopathy and age-related changes in heart size [1,2,3].