Profile
Description of Research
Heart failure is a clinical syndrome in which cardiac output is insufficient to meet the body’s needs for blood and oxygen. The causes of HF include the inability of the heart to regenerate after an injury and pathological remodelling of the left ventricular wall due to increased mechanical load from hypertension or post-infarction scarring cardiac tissue in response to overload. The research at the Talman lab aims to discover new ways to treat cardiac diseases by investigating the molecular mechanisms of cardiac regeneration and remodelling and thereby identifying new potential drug targets. We then collaborate with chemists to develop and characterise new compounds with potential to enhance the regenerative capacity of the heart or to inhibit cardiac remodelling. We also develop and characterise physiologically relevant hPSC-based in vitro models for cardiac diseases to allow mechanistic and drug discovery research.
Representative Publications
Majid QA, Ghimire BR, Merkely B, Randi AM, Harding SE, Talman V*, Földes G* (2024): Generation and characterisation of scalable and stable human pluripotent stem-cell derived microvascular-like endothelial cells for cardiac applications. Angiogenesis 27: 561-582. https://doi.org/10.1007/s10456-024-09929-5
Pohjolainen L, Kinnunen SM, Auno S, Kiriazis A, Pohjavaara S, Kari-Koskinen J, Zore M, Jumppanen M, Yli-Kauhaluoma J, Talman V, Ruskoaho H, Välimäki M (2024): Switching hypertrophic signalling towards enhanced cardiomyocyte maturity by GATA4-targeted compound. Stem Cell Res Ther 15:5. https://doi.org/10.1186/s13287-023-03623-x
Chaudhari U, Pohjolainen L, Ruskoaho H, Talman V (2023): Genome-wide profiling of miRNA-gene regulatory networks in mouse postnatal heart development – implications for cardiac regeneration. Front Cardiovasc Med, 10:1148618. https://doi.org/10.3389/fcvm.2023.1148618
Pohjolainen L, Ruskoaho H, Talman V (2022) Transcriptomics reveal stretched human pluripotent stem cell-derived cardiomyocytes as an advantageous hypertrophy model. J Mol Cell Cardiol Plus, 2:100020. https://doi.org/10.1016/j.jmccpl.2022.100020
Karhu ST, Ruskoaho H, Talman V (2021) Distinct regulation of cardiac fibroblast proliferation and transdifferentiation by classical and novel protein kinase C isoforms: possible implications for new antifibrotic therapies. Mol Pharmacol, 99:104-113. https://doi.org/10.1124/molpharm.120.000094