Early-aging conditions and their link to artery disease
Premature aging disorders, metabolites, and atherosclerosis
['FUNDING_R01'] · UNIVERSITY OF TX MD ANDERSON CAN CTR · NIH-11228780
This project looks for ways to stop early-aging from radiation or progeria from causing artery blockage and heart disease in cancer survivors and people with progeria.
Quick facts
| Phase | ['FUNDING_R01'] |
|---|---|
| Study type | Nih_funding |
| Sex | All |
| Sponsor | UNIVERSITY OF TX MD ANDERSON CAN CTR (nih funded) |
| Locations | 1 site (HOUSTON, UNITED STATES) |
| Trial ID | NIH-11228780 on ClinicalTrials.gov |
What this research studies
Researchers will study how premature aging of blood vessel cells—caused by ionizing radiation in cancer treatment or by Hutchinson-Gilford progeria—speeds up hardening and blockage of the arteries. They will examine molecular steps inside endothelial cells, focusing on mitochondrial reactive oxygen, a signaling protein called PKCζ, loss of TOP2β, and activation of PARP that together trigger a harmful secretory state. The team will also analyze small-molecule changes in these cells using mass‑spec metabolite profiling to find affected pathways like GAGs, glutamate, and NAD+/hydrogen sulfide. Findings may point to targets for drugs or interventions to prevent or slow artery disease linked to premature aging.
Who could benefit from this research
Good fit: Ideal candidates are cancer survivors exposed to ionizing radiation who have signs of accelerated vascular aging and people with Hutchinson-Gilford progeria syndrome or similar premature-aging conditions.
Not a fit: People whose artery disease is caused primarily by unrelated factors (for example, only long-term cholesterol-driven disease or advanced, irreversible blockages) may not benefit directly from these specific findings.
Why it matters
Potential benefit: If successful, this work could point to new treatments that prevent or slow atherosclerosis and coronary disease in people who experience premature vascular aging, such as cancer survivors and individuals with progeria.
How similar studies have performed: Related work has linked mitochondrial ROS, PARP, and some metabolite pathways to vascular damage, but the specific PKCζ–TOP2β–PISP mechanism and combined metabolite findings are a novel approach.
Where this research is happening
HOUSTON, UNITED STATES
- UNIVERSITY OF TX MD ANDERSON CAN CTR — HOUSTON, UNITED STATES (ACTIVE)
Researchers
- Principal investigator: ABE, JUN-ICHI — UNIVERSITY OF TX MD ANDERSON CAN CTR
- Study coordinator: ABE, JUN-ICHI
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.
Conditions: Atherosclerotic Cardiovascular Disease, Cancer Survivor, Cardiovascular Diseases