Yukun Zhang
Senior author of a study showing that failing chaperone-mediated autophagy lets midnolin accumulate and degrade TSC2, overactivating mTORC1 and accelerating intervertebral disc degeneration
Department of Orthopedics · Union Hospital, Tongji Medical College · Huazhong University of Science and Technology · Wuhan, China
Portrait: Union Hospital, Tongji Medical College, Huazhong University of Science and Technology
Yukun Zhang is a corresponding/senior author in the spine research group at Union Hospital, Wuhan. The team showed that in degenerating intervertebral discs, a quality-control pathway (chaperone-mediated autophagy) fails, letting the protein Midnolin (MIDN) pile up; accumulated MIDN then binds and destroys TSC2, the brake on mTORC1. With that brake gone, mTORC1 hyperactivates, pushing disc cells into senescence and breaking down the disc's extracellular matrix. Restoring autophagy, removing MIDN, or directly inhibiting mTORC1 with rapamycin each attenuated the damage.
PubMed lists Zhang as corresponding author on multiple other 2026 Union Hospital papers on disc-degeneration biomaterials and cell therapy, indicating an active role in this hospital's intervertebral-disc-degeneration research.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2026 | A | Impaired Chaperone-Mediated Autophagy Accelerates Intervertebral Disc Degeneration by Inducing MIDN Accumulation to Target TSC2 for Proteasomal Degradation CHEN2026C Senior/corresponding author on the Union Hospital study defining the impaired-CMA → MIDN accumulation → TSC2 degradation → mTORC1 hyperactivation axis in intervertebral disc degeneration. |
Co-authors in the Atlas 1
People with a profile here who share at least one study with Yukun Zhang.
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- Xianglong Chen Orthopedic researcher at Union Hospital, Wuhan, and first author of a 2026 study that found a new route by which failing autophagy switches on mTORC1 and drives spinal disc degeneration
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