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Department of Physiology and Pharmacology

Mohammad Yunus Ansari, Ph.D.

Mohammad Yunus Ansari, Ph.D.

Associate Professor
Department of Physiology and Pharmacology
Department of Orthopaedic Surgery
419.383.4468
Mohammad.Ansari@暗网禁区.edu听

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Dr. Mohammad Yunus Ansari is a tenure-track Associate Professor in the Department of Physiology and Pharmacology, College of Medicine and Life Sciences, at the University of Toledo, with a secondary appointment in the Department of Orthopedic Surgery. He received his Ph.D. in Virology from the Indian Institute of Science (IISc), India. He completed his first postdoctoral training at the International Centre for Genetic Engineering and Biotechnology (ICGEB), India, and subsequently joined Northeast Ohio Medical University (NEOMED) as a postdoctoral fellow, where he progressed through the academic ranks to become a Research Assistant Professor. Prior to joining the University of Toledo, Dr. Ansari served as a tenure-track Assistant Professor at NEOMED. Dr. Ansari directs the Spine and Joint Health Research Lab, which focuses on understanding the role of mitochondrial biology on oxidative stress, inflammation, and pain in osteoarthritis and intervertebral disc degeneration. He has extensive experience in musculoskeletal biology, has published in leading peer-reviewed journals, and is currently funded by NIAMS/NIH. Dr. Ansari also developed a novel high-resolution contrast-enhanced microCT imaging approach for intervertebral discs and holds a related patent application. He is committed to advancing translational research, mentoring trainees, and fostering interdisciplinary collaboration.

Research Interest

Dr. Mohammad Ansari is a molecular biologist with a Ph.D. in virology and extensive expertise in mitochondrial biology, innate immune signaling, autophagy-lysosomal pathways, and non-coding RNA regulation in chronic inflammatory diseases. The lab鈥檚 research centers on how mitochondrial dysfunction, especially mitochondrial DNA damage and cytosolic mtDNA release activates inflammatory pathways such as cGAS/STING to promote inflammation, cellular senescence, tissue degeneration, and pain. Using genetically modified mouse models, advanced imaging approaches, and state-of-the-art molecular and biochemical techniques, the lab aims to define disease-driving mechanisms and identify novel therapeutic targets.

Ansari lab also works on developing novel contrast agents for cartilage and intervertebral disc imaging. We recently developed and validated a novel contrast-enhanced micro-computed tomography (micro-CT) approach to visualize the nucleus pulposus (NP) and overall intervertebral disc (IVD) structure in three dimensions with unprecedented clarity (). Using potassium iodide (KI) as a reversible contrast agent, our study demonstrated enhanced X-ray attenuation of the NP across multiple animal models, including mouse, rat, rabbit, and sheep discs, enabling high-resolution quantification of disc height and NP volume without compromising downstream histological or immunostaining analyses. This imaging platform overcomes a major barrier in IVD research by providing a non-destructive, 3D quantitative tool for assessing disc morphology and degeneration, creating a foundation for longitudinal studies and therapeutic evaluations.

Professional memberships

  • Orthopaedic Research Society (ORS)
  • American Physiological Society (APS)

Funding

  • 1R01AR086165-01听 Mohammad Yunus Ansari (PI) 09/15/2025-08/31/2030)
  • Title: mitochondrial DNA leakage promotes inflammation and intervertebral disc degeneration
  • Role: Principal Investigator (PI)
  • The goal of this proposal is to investigate the mechanism of mtDNA leakage and inflammation in intervertebral disc degeneration.

Appointments and Positions

  • 2026 - Associate Professor (Tenure Track), University of Toledo/Physiology and Pharmacology, Toledo, OH, United States
  • 2026 - Associate Professor, University of Toledo/Orthopaedic Surgery, Toledo, Ohio, United States
  • 2022 - 2025 Assistant Professor (Tenure Track), Northeast Ohio Medical University/Biomedical Sciences, Rootstown, Ohio, United States
  • 2019 - 2022 Assistant Professor Research, Northeast Ohio Medical University/Biomedical Sciences, Rootstown, Ohio, United States
  • 2018 - 2019 Research Scientist, Northeast Ohio Medical University/Biomedical Sciences, Rootstown, Ohio, United States
  • 2014 - 2017 Postdoctoral Research Fellow, Northeast Ohio Medical University/Biomedical Sciences, Rootstown, Ohio, United States
  • 2012 - 2014 Postdoctoral Research Fellow, International Centre for Genetic Engineering and Biotechnology, New Delhi, Delhi, India

Spine and Joint Health Research Lab

Welcome to the Spine & Joint Health Laboratory in the Department of Physiology and Pharmacology at The University of Toledo. Our lab focuses on understanding the molecular and cellular mechanisms underlying musculoskeletal diseases, with particular emphasis on osteoarthritis and intervertebral disc degeneration.

We have extensive expertise in musculoskeletal biology and a strong track record of publications in leading peer-reviewed journals. Our research is centered on elucidating how mitochondrial dysfunction drives oxidative stress, inflammatory signaling, and pain pathways, contributing to tissue degeneration. A key strength of the lab is the integration of mechanistic biology with advanced technologies.

Our work is supported by funding from the NIH/NIAMS and is driven by a commitment to translational research, interdisciplinary collaboration, and the mentorship of trainees. Through these efforts, we aim to advance the development of innovative methods and therapeutic strategies for degenerative spine and joint diseases.

Current projects

Contrast enhanced imaging of intervertebral disc

We recently developed and validated a novel contrast-enhanced micro-computed tomography (micro-CT) approach to visualize the nucleus pulposus (NP) and overall intervertebral disc (IVD) structure in 3D with unprecedented clarity. Using potassium iodide (KI) as a reversible contrast agent, we demonstrated enhanced X-ray attenuation by the NP across multiple animal models, including mouse, rat, rabbit, and sheep discs, enabling high-resolution quantification of disc height and NP volume without compromising downstream histological or immunostaining analyses. KI staining faithfully detected degenerative changes in the NP in both needle-puncture injury and aging models, matching histopathological features and facilitating robust, quantitative assessments of IVD degeneration. This imaging platform overcomes a major barrier in IVD research by providing a non-destructive, 3D quantitative tool for assessing disc morphology and degeneration, creating a foundation for longitudinal studies and therapeutic evaluations.

High-Resolution 3-Dimensional Micro-CT Imaging of Intervertebral Discs Using a Novel Contrast Agent

Reference: Buckles et al; High-Resolution 3-Dimensional Micro-CT Imaging of Intervertebral Discs Using a Novel Contrast Agent, JOR Spine, 2025 Oct 7;8(4):e70125

Mitochondrial dynamics in Osteoarthritis and intervertebral disc degeneration

Emerging evidence highlights the central role of mitochondrial dynamics, including fusion, fission, and mitophagy, in the pathogenesis of osteoarthritis (OA). This study synthesizes current understanding of how disruptions in mitochondrial homeostasis contribute to cartilage degeneration and joint pathology. In healthy chondrocytes, a tightly regulated balance between mitochondrial fusion and fission maintains bioenergetic function and cellular resilience. However, in OA, this balance is disrupted, leading to excessive mitochondrial fragmentation, impaired mitophagy, and accumulation of dysfunctional mitochondria. These alterations drive increased production of reactive oxygen species (ROS), mitochondrial DNA damage, and activation of inflammatory signaling pathways, ultimately promoting chondrocyte apoptosis, senescence, and extracellular matrix degradation. Key regulatory proteins governing mitochondrial dynamics, including those involved in fission (e.g., DRP1) and fusion (e.g., MFN1/2, OPA1), are dysregulated in OA, further exacerbating disease progression. Importantly, targeting mitochondrial quality control mechanisms by restoring mitophagy, reducing oxidative stress, or modulating the balance of fusion and fission represents a promising therapeutic strategy. This work underscores mitochondrial dynamics as a critical mechanistic link between cellular stress, inflammation, and tissue degeneration in OA, aligning with efforts to develop disease-modifying interventions.

ERK1/2-mediated activation of DRP1 regulates mitochondrial dynamics and apoptosis in chondrocytes

Reference: Ansari et al, ERK1/2-mediated activation of DRP1 regulates mitochondrial dynamics and apoptosis in chondrocytes, Osteoarthritis Cartilage, 2022 Feb;30(2):315-328

Selected Publications

  1. Buckles MM, Nur A, Warda NH, Moncher JC, Ansari MY. High-Resolution 3-Dimensional Micro-CT Imaging of Intervertebral Discs Using a Novel Contrast Agent. JOR Spine. 2025 Oct 7;8(4):e70125. doi: 10.1002/jsp2.70125. eCollection 2025 Dec.
  2. Ansari, M.Y., Novak K., and Haqqi T.M. ERK1/2-mediated activation of DRP1 regulates mitochondrial dynamics and apoptosis in chondrocytes. Osteoarthritis Cartilage, 30, 315-328, PMID: 34767958 (IF: 6.576).
  3. Ansari, M. Y., Ball, H. C., Wase, S. W., Novak, K., Haqqi, T.M. Lysosomal dysfunction in osteoarthritis and aged cartilage triggers apoptosis in chondrocytes through Bax mediated release of Cytochrome c鈥�.Osteoarthritis Cartilage, 29, 100-112, PMID:33161099. (IF: 6.576).
  4. Daniel J., Klionsky et al. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition). Autophagy,1-382, PMID:33634751 (IF:16.016).
  5. Ansari, M. Y., Ahmad, N., Voleti, S., Wase, S. W., Novak, K., Haqqi, T.M. Mitochondrial dysfunction triggers catabolic response in chondrocytes via ROS mediated activation of JNK/AP1 pathway. J Cell Sci, 30, 133(22), PMID:33097606 (IF:5.285)
  6. Ansari, M. Y., Ahmad, N., and Haqqi, T. M. Oxidative stress and inflammation in osteoarthritis pathogenesis: Role of polyphenols. Biomed Pharmacother 129, 110452, PMID:32768946 (IF:6.52)
  7. Ahmad, N., Ansari, M. Y., Bano, S., Haqqi T. M., Imperatorin suppresses IL-1 beta-induced iNOS expression via inhibiting ERK-MAPK/AP1 signaling in primary human OA chondrocytes. Int Immunopharmacol 85, 106612, PMID:32450530 (IF:4.93)
  8. Ansari, M. Y., Khan, N. M., Ahmad, N., Green J, Novak K. and Haqqi T.M. Genetic inactivation of ZCCHC6 suppresses Interleukin-6 expression and reduces the severity of experimental osteoarthritis in mice. Arthritis Rheumatol 71, 583-593, PMID:30302948 (IF:10.995)
  9. Ansari, M. Y., Ahmad, N., and Haqqi, T. M. Butein activates autophagy through AMPK/TSC2/ULK1/mTOR pathway to inhibit IL-6 expression in IL-1beta stimulated human chondrocytes. Cell Physiol Biochem 49, 932-946, PMID:30184535 (IF:5.14)
  10. Ansari, M. Y., Khan, N. M., Ahmad, I., and Haqqi T.M. Parkin clearance of dysfunctional mitochondria regulates ROS levels and increases survival of human chondrocytes. Osteoarthritis Cartilage 26, 1087-1097, PMID:28801211 (IF: 6.576)
  11. Ansari, M. Y., and Haqqi, T. M. Interleukin-1beta induced stress granules sequester COX-2 mRNA and regulates its stability and translation in human OA chondrocytes. Sci Rep 6, 27611, PMID:27271770 (IF:4.37)
  12. Chauhan, A., Zubair, S., Nadeem, A., Ansari, S.A., Ansari, M.Y., and Mohammad, O. Escheriosome-mediated cytosolic delivery of PLK1-specific siRNA: potential in treatment of liver cancer in BALB/c mice. Nanomedicine (Lond) 9, 407-420, PMID:24910873 (IF:5.3)听

Book Chapter

  1. Ansari, M.Y. and Haqqi T.M. Assessing chondrocyte status by immunofluorescence-mediated localization of Parkin relative to mitochondria. Methods Mol Biol 2245, 215-224, PMID:33315205