Research summary
Outputs centre on cardiac biology and microRNA regulation of cardiac stress, growth, and regeneration. Partial surgical resection of 1-day-old neonatal mouse hearts elicited regeneration via cardiomyocyte proliferation with minimal hypertrophy or fibrosis, a capacity lost by 7 days of age; genetic fate mapping confirmed that pre-existing cardiomyocytes (not progenitors) provided the regenerated tissue, distinguishing this response from scar-forming repair in the adult [1]. A signature pattern of stress-responsive microRNAs (>12 miRNAs up- or down-regulated by transverse aortic constriction or activated calcineurin) was identified as both correlate and effector of pathological cardiac remodelling, with several miRNAs sufficient to evoke hypertrophy and heart failure when overexpressed [4]. The intronic miR-208, encoded within the alpha-MHC gene, was shown to be required for cardiomyocyte hypertrophy, fibrosis, and stress-induced beta-MHC upregulation in response to mechanical and hormonal signalling, revealing that the alpha-MHC locus regulates cardiac growth in addition to encoding a contractile protein [3]. In a parallel post-MI context, dysregulated miRNAs (including downregulated miR-29 family members in the infarct border zone) were shown to control cardiac fibrosis in both mice and humans, with miR-29 derepression upregulating fibrotic gene programs [2]. The Cardiac Hypertrophy review framed hypertrophy as the heart's response to extrinsic and intrinsic biomechanical stress and argued that, in most cases, it is maladaptive rather than compensatory, motivating therapeutic strategies that modulate myocardial growth without impairing contractility [5]. Methodologically the work pairs murine genetic and surgical injury models with miRNA profiling, gain-of-function transgenics, and fate mapping to dissect post-transcriptional regulation of cardiac stress responses.
Recent publications
- Transient Regenerative Potential of the Neonatal Mouse HeartDOI
- A Calcineurin-Dependent Transcriptional Pathway for Cardiac HypertrophyDOI
- Transcriptional co-activator PGC-1伪 drives the formation of slow-twitch muscle fibresDOI
- The many roles of histone deacetylases in development and physiology: implications for disease and therapyDOI
- Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosisDOI
- The Endothelial-Specific MicroRNA miR-126 Governs Vascular Integrity and AngiogenesisDOI
- MicroRNAs in Stress Signaling and Human DiseaseDOI
- Control of Stress-Dependent Cardiac Growth and Gene Expression by a MicroRNADOI
- A signature pattern of stress-responsive microRNAs that can evoke cardiac hypertrophy and heart failureDOI
- Cardiac Hypertrophy: The Good, the Bad, and the UglyDOI
The lab page does not clearly state student acceptance status. Email the professor directly to confirm.
How to apply
Email Eric N. Olson 6-12 months before your application deadline. Read several recent papers and reference specific work in your message. Use our how to email a Japanese professor guide for the proven email structure.
For applications via MEXT scholarship: see our MEXT 2027 complete guide and university-specific University Recommendation track.
External profiles
- ORCID: https://orcid.org/0000-0003-1151-8262
- OpenAlex: openalex.org
Profile compiled from public sources (Researchmap, OpenAlex, The University of Tokyo faculty directory). Last refreshed 2026-05. Report incorrect information.