Joona Valtonen

ORCID: 0000-0003-2704-4663
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About
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Research Areas
  • Cardiomyopathy and Myosin Studies
  • Liver Disease Diagnosis and Treatment
  • Lymphatic System and Diseases
  • MicroRNA in disease regulation
  • Allergic Rhinitis and Sensitization
  • Anesthesia and Neurotoxicity Research
  • Asthma and respiratory diseases
  • Immunotherapy and Immune Responses
  • Anesthesia and Sedative Agents
  • CRISPR and Genetic Engineering
  • Cardiac, Anesthesia and Surgical Outcomes
  • Erythrocyte Function and Pathophysiology
  • Cell Adhesion Molecules Research
  • Tissue Engineering and Regenerative Medicine
  • Galectins and Cancer Biology
  • Caveolin-1 and cellular processes
  • Electrospun Nanofibers in Biomedical Applications
  • Immune Response and Inflammation
  • Viral Infections and Immunology Research
  • Liver physiology and pathology
  • Hippo pathway signaling and YAP/TAZ
  • Circular RNAs in diseases
  • 3D Printing in Biomedical Research

Tampere University
2021-2024

University of Turku
2012-2016

Turku University Hospital
1994

Finnish Red Cross
1984

Significance Organ fibrosis is a major cause of global morbidity and mortality. It driven by chronic inflammation associated oxidative stress with depletion cellular antioxidant defenses. We demonstrate pathway in which the evolutionarily conserved receptor stabilin-1 on tissue-infiltrating macrophages provides second-line defense to prevent tissue damage from stress. Stabilin-1 + monocytes take up malondialdehyde-LDL (MDA-LDL), product lipid peroxidation, form ceroid-laden macrophages....

10.1073/pnas.1604780113 article EN Proceedings of the National Academy of Sciences 2016-07-29

Abstract Cardiovascular diseases remain as the most common cause of death worldwide. To reveal underlying mechanisms in varying cardiovascular diseases, vitro models with cells and supportive biomaterial can be designed to recapitulate essential components human heart. In this study, we analyzed whether 3D co-culture cardiomyocytes (CM) vascular network adipose tissue-derived mesenchymal stem/stromal (ASC) support CM functionality. were cultured either endothelial (EC) ASC or only...

10.1007/s10616-024-00630-5 article EN cc-by Cytotechnology 2024-05-02

Abstract Aeroallergen provocation induces the rapid accumulation of CD11c+MHC class II (MHC II)+ dendritic cells (DCs) in lungs, which is driven by an increased recruitment blood-derived DC precursors. Recent data show, however, that well-differentiated DCs proliferate situ various tissues. This may also contribute to their allergen-induced expansion; therefore, we studied proliferation airways mice steady state and after local aeroallergen provocation. Confocal whole-mount microscopy was...

10.4049/jimmunol.1200220 article EN The Journal of Immunology 2012-12-25

Hypertrophic cardiomyopathy (HCM) is one of the most common genetic cardiac diseases; it primarily caused by mutations in sarcomeric genes. However, HCM also associated with non-sarcomeric proteins and a Finnish founder mutation for protein junctophilin-2 (JPH2) has been identified. This study aimed at assessing issue modelling rare cardiomyocytes (CMs) differentiated from iPSCs; therefore, presenting same abnormalities observed patients. To explore abnormal functions JPH2-HCM, skin...

10.3390/biomedicines11061558 article EN cc-by Biomedicines 2023-05-27

Metabolic dysfunction, partly driven by altered liver function, predisposes to coronary artery disease (CAD), but the role of in vulnerable atherosclerotic plaque development remains unclear. Here we produced hepatocyte-like cells (HLCs) from 27 induced pluripotent stem cell (iPSC) lines derived 15 study subjects with stable CAD (n = 5), acute 5) or healthy controls 5). We performed a miRNA microarray screening throughout differentiation, as well compared iPSC-HLCs profiles patient groups...

10.1038/s41598-023-28981-7 article EN cc-by Scientific Reports 2023-01-30

Hypertrophic cardiomyopathy (HCM) is one of the most common genetic cardiac diseases primarily caused by mutations in sarcomeric genes. However, HCM also associated with non-sarcomeric proteins and a Finnish founder mutation for protein junctophilin-2 (JPH2) has been identified. MYK-461 recently described mechanistically novel small molecule that acts at sarcomere to specifically inhibit contractility proposed as treatment HCM. Here, we use test whether direct reduction sufficient relieve...

10.1161/circ.146.suppl_1.10925 article EN Circulation 2022-11-08
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