Key result
Multi-network comparative analysis of the transcriptome and translatome in mouse models of cardiac remodeling identified novel hub genes, including Fam210a and Psmd12.
Why the study?
The transition from physiological to pathological cardiac hypertrophy remains elusive and largely based on reductionist hypotheses.
Multi-network analysis of mouse hearts reveals novel hub genes and significant post-transcriptional regulation during early cardiac remodeling.
Hypothesis-generating for hub genes in early cardiac remodeling; leaves open translation to human disease or therapy.
Our understanding of the transition from physiological to pathological cardiac hypertrophy remains elusive and largely based on reductionist hypotheses. Here, we profiled the translatomes of 15 mouse hearts to provide a molecular blueprint of altered gene networks in early cardiac remodeling. Using co-expression analysis, we showed how sub-networks are orchestrated into functional modules associated with pathological phenotypes. We discovered unappreciated hub genes, many undocumented for their role in cardiac hypertrophy, and genes in the transcriptional network that were rewired in the translational network, and associated with semantically different subsets of enriched functional terms, such as Fam210a , a novel musculoskeletal modulator, or Psmd12 , implicated in protein quality control. Using their correlation structure, we found that transcriptome networks are only partially reproducible at the translatome level, providing further evidence of post-transcriptional control at the level of translation. Our results provide novel insights into the complexity of the organization of in vivo cardiac regulatory networks.
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Boileau et al. (2020) studied Cardiac remodeling (n=15). Transverse aortic constriction (TAC) or swimming vs. Each other was evaluated on Identification of co-expression networks and hub genes. Multi-network comparative analysis of the transcriptome and translatome in mouse models of cardiac remodeling identified novel hub genes, including Fam210a and Psmd12.
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