Riku
Kiviranta
Docent, Institute of Biomedicine
Assistant Professor in Endocrinology and Metabolic Diseases, Consultant in Endocrinology
Contact
Links
Areas of expertise
Endocrinology
Skeletal biology
Bone metabolism
Metabolic bone diseases
Osteoporosis
Cancer
Sarcoma
Molecular biology
Signaling
Epigenetics
Biography
Dr. Kiviranta graduated as an M.D. at the University of Turku in 2010 and received his Ph.D. at the Department of Medical Biochemistry and Genetics , University of Turku in 2014 After a year of clinical work in the Department of Medicine at the Turku University Hospital he joined professor Roland Baron’s research group as a postdoctoral fellow at the Yale University School of Medicine, New Haven, CT, USA in 2015 until 2017. In 2018 professor Baron was recruited to Harvard School of Dental Medicine, Harvard University, Boston, MA, USA, and Dr. Kiviranta continued his postdoctoral work at Harvard Medical School until 2010.
In 2010 Dr. Kiviranta joined Turku Collegium of Science and Medicine at the University of Turku and began to establish his own research group in the Institute of Biomedicine at the University of Turku. He also continued his residency and fellow training in Endocrinology. Dr. Riku Kiviranta received board certification of Endocrinology in 2015. He was named Adjunct Professor (Docent) in Molecular Medicine in 2013 and as an Assistant Professor in Endocrinology and Metabolic Diseases (tenure track) in 2018. Assistant Professor Kiviranta currently works as a Clinical Endocrinologist at the Turku University Hospital and leads his research group in the Institute of Biomedicine and in the Department of Clinical Medicine.
In 2010 Dr. Kiviranta joined Turku Collegium of Science and Medicine at the University of Turku and began to establish his own research group in the Institute of Biomedicine at the University of Turku. He also continued his residency and fellow training in Endocrinology. Dr. Riku Kiviranta received board certification of Endocrinology in 2015. He was named Adjunct Professor (Docent) in Molecular Medicine in 2013 and as an Assistant Professor in Endocrinology and Metabolic Diseases (tenure track) in 2018. Assistant Professor Kiviranta currently works as a Clinical Endocrinologist at the Turku University Hospital and leads his research group in the Institute of Biomedicine and in the Department of Clinical Medicine.
Research
Bone tissue is a dynamic endocrine organ that consists of several different cell types, the bone cells (osteoblasts, osteocytes and osteoclasts), the hematopoietic stem cells (HSCs) and their off spring, as well as bone marrow adipocytes. The complex interplay between these different cell types within the bone marrow microenvironment is essential for normal bone metabolism and bone strength and for the regulatory functions of bone tissue. Loss of normal control of the differentiation process of skeletal cells may lead to the development of osteo- or chondrosarcomas that are the most common primary malignant tumors of bone. Despite advances in the surgical treatment of skeletal sarcomas, there has been very little progress in other treatment options for these tumors.
Our research group is interested in the molecular mechanisms of these abundant cellular interactions. Moreover, we focus to unravel the essential signaling pathways that control bone cell differentiation and their mechanisms of action both on the broader chromatin landscape as well as at the promoter level. We are also working to characterize the functions and metabolic roles of bone marrow adipocytes.
Currently we have two specific areas of interest: the role of Wnt signaling and its mechanisms of action in regulating bone remodeling and the role of epigenetic regulation in the control of osteoblast differentiation and in the development of skeletal sarcomas. In both of these projects we combine clinical data and samples with modern cell and molecular biologic approaches in vitro and in genetically modified animal models.
Ultimately, our goal is to identify novel therapeutic targets and approaches for metabolic and malignant bone diseases.
Our research group is interested in the molecular mechanisms of these abundant cellular interactions. Moreover, we focus to unravel the essential signaling pathways that control bone cell differentiation and their mechanisms of action both on the broader chromatin landscape as well as at the promoter level. We are also working to characterize the functions and metabolic roles of bone marrow adipocytes.
Currently we have two specific areas of interest: the role of Wnt signaling and its mechanisms of action in regulating bone remodeling and the role of epigenetic regulation in the control of osteoblast differentiation and in the development of skeletal sarcomas. In both of these projects we combine clinical data and samples with modern cell and molecular biologic approaches in vitro and in genetically modified animal models.
Ultimately, our goal is to identify novel therapeutic targets and approaches for metabolic and malignant bone diseases.
Publications
Mesenchymal cell-derived Wnt1 signaling regulates subchondral bone remodeling but has no effects on the development of growth plate or articular cartilage in mice (2022)
BONE
(Vertaisarvioitu alkuperäisartikkeli tai data-artikkeli tieteellisessä aikakauslehdessä (A1))
Treatment with Soluble Activin Type IIB Receptor Ameliorates Ovariectomy-Induced Bone Loss and Fat Gain in Mice (2022)
Calcified Tissue International
(Vertaisarvioitu alkuperäisartikkeli tai data-artikkeli tieteellisessä aikakauslehdessä (A1))
Lysine-Specific Demethylase 1 (LSD1) epigenetically controls osteoblast differentiation (2022)
PLoS ONE
(Vertaisarvioitu alkuperäisartikkeli tai data-artikkeli tieteellisessä aikakauslehdessä (A1))
Age-Progressive and Gender-Dependent Bone Phenotype in Mice Lacking Both Ebf1 and Ebf2 in Prrx1-Expressing Mesenchymal Cells (2022)
Calcified Tissue International
(Vertaisarvioitu alkuperäisartikkeli tai data-artikkeli tieteellisessä aikakauslehdessä (A1))
Early B-cell Factor1 (Ebf1) promotes early osteoblast differentiation but suppresses osteoblast function (2021)
BONE
(Vertaisarvioitu alkuperäisartikkeli tai data-artikkeli tieteellisessä aikakauslehdessä (A1))
Human Bone Marrow Adipose Tissue is a Metabolically Active and Insulin-Sensitive Distinct Fat Depot (2020)
Journal of Clinical Endocrinology and Metabolism
(Vertaisarvioitu alkuperäisartikkeli tai data-artikkeli tieteellisessä aikakauslehdessä (A1))
Mesenchymal Cell-Derived Juxtacrine Wnt1 Signaling Regulates Osteoblast Activity and Osteoclast Differentiation (2019)
Journal of Bone and Mineral Research
(Vertaisarvioitu alkuperäisartikkeli tai data-artikkeli tieteellisessä aikakauslehdessä (A1))
Cathepsin K-deficient osteocytes prevent lactation-induced bone loss and parathyroid hormone suppression (2019)
Journal of Clinical Investigation
(Vertaisarvioitu alkuperäisartikkeli tai data-artikkeli tieteellisessä aikakauslehdessä (A1))
Cilia-related protein SPEF2 regulates osteoblast differentiation (2018)
Scientific Reports
(Vertaisarvioitu alkuperäisartikkeli tai data-artikkeli tieteellisessä aikakauslehdessä (A1))
Soluble activin type IIB receptor improves fracture healing in a closed tibial fracture mouse model (2017)
PLoS ONE
(Vertaisarvioitu alkuperäisartikkeli tai data-artikkeli tieteellisessä aikakauslehdessä (A1))