Our work links osteoarthritis biology, environmental exposure stress, human joint organoids, and targeted gene/cell therapy. The goal is translation: catch degeneration early, stabilize the joint, and regenerate structure before “wait for surgery” becomes the only option.
Everything below is an active build. This is not generic review text. These are the systems we are constructing and evaluating right now.
Each program feeds data into the others. The exposure biology platform stresses the system. The joint organoids let us observe failure in real time. The repair strategy aims to fix it — and do it in a way that's actually compatible with human delivery.
We map how cartilage erodes under mechanical load + chronic inflammation, and how synovial immune activity drives or accelerates that damage.
Target: not just pain control. Structural stability and functional preservation of the native joint.Real joints operate in a toxic, high-load world. We apply pollutant mixes, overload cycles, and microinflammatory insults to recreate that pressure and watch what fails first.
Clinical angle: link exposure signatures to early-onset osteoarthritis risk and faster degeneration timelines.We grow multicellular “mini-joint” systems from human stem cells — including cartilage-like and synovium-like compartments — so we can see degeneration and repair in a controlled human-relevant model (no animal surgery).
These organoids become screening platforms for repair strategies.We prototype delivery of regenerative cells and gene-modulated factors directly to damaged joint regions, aiming to calm inflammation and resurface eroding cartilage.
Goal: a path to regulated clinical intervention, not a science project.Every study follows a tight loop: build the human model, injure it in a way that matches reality, test a repair strategy. We don’t guess. We watch it happen.
We generate multicellular joint organoids from human stem cells. These include cartilage-like and synovial-like layers so we can see how local inflammation and load interact.
Output: baseline joint health readout.We expose the model to defined pollutant mixtures, repetitive load, or inflammatory signals that mimic high-risk human environments.
Output: early cartilage breakdown + inflammatory signature.We deliver regenerative cell payloads or targeted gene modulation to see if we can stabilize tissue, suppress inflammatory damage, and resurface eroding areas.
Output: functional recovery / structural preservation.Below is a placeholder figure. Replace with your confocal snapshot, stress timeline schematic, or response heatmap. Each figure should be accessible (alt text, caption, timestamp).
We actively share organoid models, exposure assays, and regenerative repair concepts. We’re especially interested in early-stage joint degeneration (pre-surgery), high-load injury models, and controlled delivery of repair payloads.
Email a short intro with: your field, the idea you want to test, and what resource you need (model system, assay, dataset, co-development).
Private area for registered collaborators only. Access requires institutional affiliation and authenticated ORCID iD. Pre-publication data and draft protocols may be shared under NDA.