Cardiac Sex Differences are Established Prior to Gonad Formation
Shi, W.; Sheng, X.; Dorr, K. M.; Hutton, J. E.; Davies, H. A.; Andrade, T. D.; Greco, T. M.; Hashimoto, Y.; Federspiel, J. D.; Robbe, Z. L.; Chen, X.; Arnold, A. P.; Ileana M Cristea, I. M.; Conlon, F.
Show abstract
Male and female disease states differ in their prevalence, treatment responses, and survival rates. In cardiac disease, women almost uniformly fare far worse than men. Though sex plays a critical role in cardiac disease, the mechanisms underlying sex differences in cardiac homeostasis and disease remain unexplained. Here, in adult and embryonic hearts we reveal sex-specific transcriptomes and proteomes and show that cardiac sex differences are predominately accounted for by post-transcriptional mechanisms. We found differential expression of male-female proteins in the cardiomyocytes. Using a quantitative proteomics-based approach, we characterized differential sex-specific enriched cardiac proteins, protein complexes, and biological sex processes in the context of global genetic diversity of the Collaborative Cross, an established surrogate for human diversity. We also found that sex differences in cardiac protein expression are established by both hormonal and sex chromosomal mechanisms. We have demonstrated the onset of sex-biased protein expression and discovered that sex disparities in heart tissue occur at the earliest stages of heart development at a period that preceeds mammalian gonadal development. Collectively, these findings may explain why congenital heart disease, a leading cause of death whose origin is often developmental, is sex biased. Our results reveal molecular foundations for differences in cardiac tissue that underlie sex disparities in health, disease, and treatment outcomes.
Matching journals
The top 6 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- In vivo proximity labeling identifies cardiomyocyte protein networks during zebrafish heart regeneration 95%
- Cardiac pathologies in mouse loss of imprinting models are due to misexpression of H19 long noncoding RNA 95%
- The long noncoding RNA Charme supervises cardiomyocyte maturation by controlling cell differentiation programs in the developing heart 95%
Similar papers in this journal
Similar papers in this journal
Similar papers in this journal
- Simultaneous proteome localization and turnover analysis reveals spatiotemporal dynamics of unfolded protein responses 93%
- Pptc7 maintains mitochondrial protein content by suppressing receptor-mediated mitophagy 93%
- Cardiomyocyte Contractile Impairment in Heart Failure Results from Reduced BAG3-mediated Sarcomeric Protein Turnover 93%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.