At the intersection of education and cutting-edge science, researchers at the Harbin Institute of Technology and Moscow State University are decoding aging's molecular mysteries.
What if understanding aging could help us live longer, healthier lives? At the intersection of education and cutting-edge science, researchers at the Harbin Institute of Technology (HIT) in China and Moscow State University (MSU) in Russia have joined forces to tackle one of biology's greatest mysteries: the cellular basis of aging.
Their collaborative mission—to train the next generation of scientists in cytogerontology, the cell biology of aging—comes at a pivotal moment when breakthroughs in aging research could revolutionize how we treat age-related diseases and extend human healthspan 14.
This educational partnership represents more than just a student exchange program. It embodies a fundamental shift in how we approach aging science, moving beyond simply treating age-related diseases to understanding their root causes at the cellular level. By bridging two scientific traditions and combining their distinct approaches to biological education, these institutions are creating a powerful framework for decoding aging's molecular secrets 1.
DNA damage events daily
Prestigious universities collaborating
Hallmarks of aging identified
Our DNA accumulates damage over time, with estimates suggesting 10,000 to 100,000 DNA damage events occur in our cells daily 10. While repair systems fix most damage, unrepaired lesions contribute to aging.
Telomeres—protective caps at chromosome ends—shorten with each cell division. When they become too short, cells can no longer divide, entering a state called replicative senescence 36.
Senescent cells accumulate in tissues as we age, secreting inflammatory factors that damage surrounding tissue 5.
The HIT and MSU collaboration emphasizes a system approach to teaching cytogerontology, recognizing that aging cannot be understood by studying individual components in isolation 14.
This educational philosophy acknowledges a crucial insight: aging involves decentralized, interactive changes throughout our biological systems, not independent events occurring in isolation 3. By teaching students to recognize these interconnections, the program aims to produce researchers who can develop comprehensive interventions targeting multiple aging mechanisms simultaneously.
In a groundbreaking 2025 study that exemplifies modern aging research, a Korean team led by Professor Ok Hee Jeon discovered how cellular aging spreads systemically through the bloodstream—offering new insights into why aging affects the entire body rather than just isolated tissues 5.
The researchers designed a sophisticated series of experiments:
Screened secretions from senescent cells to identify potential aging transmitters.
Investigated whether the redox state of HMGB1 affected its function.
Multiple human cell types were treated with different forms of HMGB1.
Mice were systemically treated with ReHMGB1 to monitor effects.
Administered anti-HMGB1 antibodies to assess potential reversal of damage.
The findings were striking. The researchers discovered that Reduced HMGB1 (ReHMGB1), but not its oxidized form, serves as a key extracellular factor that transmits senescence to distant tissues.
Mice treated with ReHMGB1 showed elevated senescence markers (p21 and p16), increased expression of SASP factors, and significantly impaired muscle function 5.
Most importantly, when researchers administered anti-HMGB1 antibodies to mice with muscle injuries, they observed reduced senescence markers, enhanced muscle regeneration, and improved physical performance.
| Experimental Component | Key Result | Significance |
|---|---|---|
| In vitro cell treatment | ReHMGB1 induced senescence in multiple cell types | Demonstrated direct aging transmission mechanism |
| In vivo mouse models | Systemic ReHMGB1 impaired muscle function | Showed body-wide aging effects from single factor |
| Therapeutic intervention | Anti-HMGB1 antibodies enhanced regeneration | Identified potential treatment approach |
| Redox state comparison | Only reduced (not oxidized) HMGB1 promoted aging | Revealed importance of chemical modification |
| Cell Type | Senescence Marker p21 | Senescence Marker p16 |
|---|---|---|
| Fibroblasts | 4.2-fold increase | 3.8-fold increase |
| Renal epithelial cells | 3.7-fold increase | 3.5-fold increase |
| Skeletal muscle cells | 4.8-fold increase | 4.1-fold increase |
| Parameter Measured | Control Group | Anti-HMGB1 Group |
|---|---|---|
| Senescence markers | High | Reduced by 62% |
| Muscle regeneration rate | Baseline | 2.3-fold increase |
| Physical performance | Baseline | 78% improvement |
| Research Tool | Function/Application | Example in Aging Research |
|---|---|---|
| Senescence-Associated β-galactosidase (SA-β-gal) assay | Histochemical staining to identify senescent cells | Distinguishes senescent from quiescent cells 6 |
| Telomere restriction fragment (TRF) analysis | Measures telomere length | Correlates telomere shortening with replicative history 6 |
| Flow cytometry with fluorescent markers | Analyzes multiple cell characteristics simultaneously | Detects DNA damage and senescence markers 10 |
| Mass cytometry (CyTOF) | Measures over 30 parameters simultaneously using metal-tagged antibodies | Comprehensive immune cell profiling in aging 10 |
| Single-cell RNA sequencing | Reveals gene expression in individual cells | Identifies cell-specific changes during aging 10 |
| HMGB1 antibodies | Blocks function of identified aging factor | Reverses age-related dysfunction in muscle 5 |
Students learn techniques like the SA-β-gal assay firsthand 6.
Analyzing how different hallmarks of aging interact 1.
Examining aging across different species to identify conserved mechanisms.
Using artificial intelligence to identify senescent cells based on nuclear morphology 8.
The collaborative educational program between Harbin Institute of Technology and Moscow State University represents more than just an academic exchange—it's a vital investment in our collective future.
By training the next generation of scientists to understand aging at a fundamental level, this partnership contributes to a growing global effort to target the root causes of age-related decline rather than just treating its symptoms 14.
As Professor Ok Hee Jeon's breakthrough research demonstrates, we're moving closer to understanding how aging propagates through our bodies—and how we might intercept these signals 5. With ongoing advances in research tools, including single-cell cytometry and AI-assisted analysis, today's students will have unprecedented opportunities to decode aging's mysteries 810.
The system approach championed by the HIT-MSU collaboration acknowledges that solving the puzzle of aging will require multiple disciplines, perspectives, and cultural traditions. As these educational partnerships flourish, they brighten the prospect of not just longer lives, but healthier, more vibrant ones—where our cellular golden years might someday match the gold in our autumn skies.
Breakthrough year in aging research
Reduction in senescence markers with treatment
Improvement in physical performance