Education & Training:
Istanbul University Cerrahpasa Medical School, B.S. in Biomedical Sciences
University of Connecticut, M.S. and Ph.D.
Cincinnati Children’s Hospital Medical Center, Postdoctoral Fellow

Research Interests:
The overall goal of my laboratory is to understand how tissue-resident cells coordinate injury responses, tissue repair, and regeneration. We are particularly interested in fibroblast biology and how distinct fibroblast states regulate inflammation, extracellular matrix remodeling, vascular responses, and tissue recovery. Our long-term goal is to identify cell- and state-specific therapeutic targets that promote effective wound healing while preventing pathological fibrosis.

We use genetic mouse models, lineage tracing, gain- and loss-of-function approaches, single-cell technologies, and cellular and molecular interrogation to define the origin, fate, and function of fibroblasts during homeostasis and disease. A major focus of our work is understanding fibroblast plasticity. Rather than viewing activated fibroblasts simply as terminal matrix-producing cells, our studies investigate how fibroblasts transition through distinct functional states during injury and recovery, including their ability to deactivate and participate in tissue remodeling and resolution.

Our cardiovascular studies investigate the cellular mechanisms that determine whether an injured heart undergoes adaptive repair or progresses toward pathological remodeling and heart failure. We study the dynamic interactions among cardiac fibroblasts, cardiomyocytes, immune cells, and endothelial cells, with particular interest in fibroblast activation and deactivation, extracellular matrix remodeling, inflammation, angiogenesis, and cardioprotection following cardiac injury.

We extend these concepts across skeletal muscle and lung injury to identify conserved and tissue-specific mechanisms of repair. In skeletal muscle, we investigate interactions among fibroblasts, muscle stem cells, immune cells, and the vasculature that determine successful regeneration versus fibrosis. In the lung, our work has demonstrated that fibroblasts are not simply structural cells responding to tissue damage but can adopt immunomodulatory states that actively contribute to host defense during Aspergillus fumigatus infection. Together, these studies seek to define fundamental principles of cellular crosstalk that determine whether damaged tissues regenerate, resolve, or progress toward chronic fibrosis.

Selected Publications:

• • Guirao-Abad JP, Kasprovic DA, Seo D, et al., Kanisicak O. Pulmonary fibroblast activation during Aspergillus fumigatus infection enhances lung defense via immunomodulation and tissue remodeling. Nature Communications. 2026.
  • Ozdemir M, Guirao-Abad JP, Kasprovic DA, Jaggers RM, Kanisicak O. Angiotensin II promotes progressive activation of fibrogenic periostin-lineage cells in lung and kidney. Cells. 2025.
  • Slone S, Anthony SR, Green LC, et al., Kanisicak O, Tranter M. HuR inhibition reduces post-ischemic cardiac remodeling by dampening myocyte-dependent inflammatory gene expression and the innate immune response. FASEB Journal. 2025.
  • Kanisicak O, Khalil H, Ivey MJ, et al. Genetic lineage tracing defines myofibroblast origin and function in the injured heart. Nature Communications. 2016.
  • Kaur H, Takefuji M, Ngai CY, et al., Kanisicak O, et al. Targeted ablation of periostin-expressing activated fibroblasts prevents adverse cardiac remodeling in mice. Circulation Research. 2016.
    1. Guirao-Abad JP, Kasprovic DA, Seo D, Ozdemir M, Shearer SM, Wen BY, Bowden JJ, Grisham C, Wang Y, Tranter M, Askew DS, Kanisicak O. Pulmonary fibroblast activation during Aspergillus fumigatus infection enhances lung defense via immunomodulation and tissue remodeling. Nat Commun. 2026 Mar 31;17(1). doi: 10.1038/s41467-026-71027-5. PubMed PMID: 41917025; PubMed Central PMCID: PMC13201633.
    2. Mustafa Ozdemir, José P. Guirao-Abad, Daniel A. Kasprovic, Robert M. Jaggers, Onur Kanisicak. Angiotensin II Promotes Progressive Activation of Fibrogenic Periostin-Lineage Cells in Lung and Kidney. Cells. 2025 October. doi: 10.3390/cells14201584.
    3. Taejeong Song, Maicon Landim-Vieira, Mustafa Ozdemir, Caroline Gott, Onur Kanisicak, Jose Renato Pinto and Sakthivel Sadayappan. (2023). Etiology of genetic muscle disorders induced by mutations in fast and slow skeletal MyBP-C paralogs. Exp Mol Med. 2023 Mar;55(3):502-509. doi: 10.1038/s12276-023-00953-x.
    4. Alam P., Haile B., Mohammed A., Pandey R., Rokvic M., Nieman M., Maliken B. D., Paul A., Wang Y., Sadayappan S., Ahmed R. PH., and Kanisicak O. (2019) Inhibition of senescence associated genes Rb1 and Meis2 in adult cardiomyocytes results in cell cycle reentry and cardiac repair post MI. J Am Heart Assoc. 2019 Aug 6;8(15):e012089. doi: 10.1161/JAHA.119.012089.
    5. Fu X., Khalil H., Kanisicak O., Boyer J. G., Vagnozzi R. J., Maliken B. D., Sargent M. A., Prasad V, Valiente-Alandi I., Blaxall B. C., Molkentin J. D. (2018) Defining Fibroblast Differentiated States in the Infarcted Mouse Heart. J Clin Invest. 2018;128(5):2127–2143
    6. Khalil H., Kanisicak O., Prasad N., Correll R. N., Fu X., Schips T., Vagnozzi R. J., Liu R., Huynh T., Lin S. J., Karch J., Molkentin J. D. (2017) Fibroblast-specific genetic dissection of TGFβ-Smad2/3 signaling in cardiac fibrosis. J Clin Invest. (JCI-94753)
    7. Vanhoutte D., Kwong J. Q., Davis J., Schips T. G., Tjondrokoesoemo A., Brody M. J., Sargent M. A., Kanisicak O., Yi H., Gao Q. Q., Rabinowitz J. E., Volk T., McNally E. M., Molkentin J. D. (2016). Thrombospondin expression in myofibers stabilizes muscle membranes. eLife 2016;5:e17589.
    8. Kanisicak O., Khalil H., Ivey M. J., Karch J., Maliken B. D., Correll R. N., Brody M. J., Lin S. J., Aronow B. J., Tallquist M. D., Molkentin J. D. (2016). Genetic lineage tracing defines myofibroblast origin and function in the injured heart. Nat Commun. 7:12260. doi: 10.1038/ncomms12260.
    9. Tjondrokoesoemo A., Schips T. G., Kanisicak O., Sargent M. A., Molkentin J.D. (2016). Genetic overexpression of serpina3n attenuates muscular dystrophy in mice. Hum Mol Genet. 25 (6) , art. no. ddw005 , pp. 1192-1202.
    10. Accornero F, Kanisicak O., Tjondrokoesoemo A, Attia A. C., McNally E. M., Molkentin J. D. (2014). Myofiber-specific inhibition of TGFβ signaling protects skeletal muscle from injury and dystrophic disease in mice. Hum Mol Genet. 20;23(25):6903-15.
    11. Van Berlo J. H.*, Kanisicak O.*, Maillet M., Vagnozzi R. J., Karch J., Lin S. J., Middleton R. C., Marba´n E. & Molkentin J. D. (2014). c-kit+ cells minimally contribute cardiomyocytes to the heart. Nature 15;509(7500):337-41.
    12. Kanisicak O.*, Mendez J. J.*, Yamamoto S., Yamamoto M., and Goldhamer D. J. (2009). Progenitors of skeletal muscle satellite cells express the muscle determination gene, MyoD. Dev. Biol. 332, 131-141.

NCBI link: https://www.ncbi.nlm.nih.gov/myncbi/onur.kanisicak.1/bibliography/public/