Dr. Kermani received her D.V.M degree from University of Tehran Veterinary School and completed a four-year residency in Medical Microbiology, Virology, and Immunology from the University of Tehran Medical School. She received both her M.P.H. in Molecular and Hospital Epidemiology and a Ph.D. in Epidemiology Science (Virology) from the University of Michigan. Following graduation, she completed her postdoctoral training in Pathology followed by fellowship training in Molecular Medicine and Genetic and Hematology and Oncology in the Department of Internal Medicine at the University of Michigan. Then, she accepted dual positions of Adjunct Assistant Professor and Research Investigator at the University of Michigan Medical School. In addition, from 2013-2018, she worked as Assistant Professor at the Cancer Therapy Center at University of Massachusetts Boston. Since 2018, she worked as a Research Assistant Scientist in the Departments of Internal Medicine and Dermatology at University of Michigan.

She served on numerous local and national committees and is a member of many societies including American College of Rheumatology, American Society of Investigative Dermatology, American Society for Virology, American Society for Investigative Pathology, American Urology Association, and the Society for Basic Urologic Research.

Dr. Kermani has published over seventy articles in prestigious scientific journals, given over one hundred invited and other presentations at local, national, and international conferences, has over hundred published abstracts, and received sixteen awards.

Dr. Kermani's research area interests include fibrosis, autoimmunity, and cancer. She is investigating pulmonary and other types of fibrosis such as skin, kidney, liver as well as psoriasis, systemic lupus erythematosus, scleroderma, and other autoimmune diseases.
Her current research aims to define how the female-biased factor VGLL3 drives fibrosis in the skin and systemic fibrosis such as kidney, liver, and lung fibrosis.
Her most research interests' area as following:
1. Role of hippo signaling in regulation of STING activation in SLE and upregulation IFN production in SLE monocytes.

2. Role of TYK2 inhibitor BMS-986165 on SLE endothelial progenitor cells. Investigation of LINE elements in SLE.

3. Elucidation of the molecular mechanisms of fibrosis, psoriasis, dermatomyositis, tissue injury, inflammation in cutaneous lupus, organ damage in
systemic lupus erythematosus, scleroderma, atopic dermatitis, and other autoimmune diseases using ingle cell sequencing, spatial sequencing,
multiome and immunohistochemistry.

4. Identification of VGLL3 as a primary orchestrator of sex bias in autoimmune diseases, chronic inflammation, fibrosis, and cancer including, 1)
activation and repression of signaling mechanisms that engage in epithelial, fibroblast proliferation, epithelial, mesenchymal transformation, and
myofibroblast differentiation, 2) gene transcription by secreted inflammatory cytokines and chemokines in chronic inflammation; cancer, fibrotic
diseases of the skin, kidney, liver, and lung, 3) role of Hippo and TGF beta pathways in fibrosis.

5. Role of ultraviolet light in lupus, systemic lupus erythematosus, scleroderma, and psoriasis using human tissue explant model.

6. Elucidation of the molecular and cellular mechanisms involved in aging and inflammation-associated pulmonary, urinary tract and skin fibrosis,
particularly the role of TGF beta and cc-type chemokines in lung, prostate, bladder kidney fibrosis. My research has identified potential new
mechanisms through which TGF beta and cc-type chemokines mediate prostate fibrosis consequent to aging by promoting myofibroblast
differentiation and consequent extracellular matrix remodeling, resulting in increased prostate tissue stiffness and urethral dysfunction.

7. Epigenetic regulation of myofibroblast differentiation by DNA methylation; and the role of myofibroblasts in human and in animal models of fibrosis
and lupus. Evaluation of anti-fibrotic therapeutic agents to treat fibrosis such as, skin, kidney and lower urinary tract symptomatic patients who do
not respond to commonly prescribed pharmacotherapies.

8. Role of microbiome in autoimmune diseases such as systemic lupus erythematosus, psoriasis, scleroderma, lupus, and atopic dermatitis.