Children living with Hutchinson–Gilford Progeria Syndrome

HGPS Research · University of Maryland

Studying Aging
At Its Source

The Cao Lab investigates Hutchinson–Gilford Progeria Syndrome and what it reveals about the biology of aging every one of us shares.

Explore the Research
Illustration of a DNA strand highlighting a single point mutation

The Central Question

One Gene.
Two Timelines.

A single mutation in the LMNA gene compresses a lifetime of cellular aging into childhood — a rare, sharpened lens on a process every one of us goes through.

See How It Works
The Cao Lab team standing together in the lab

From Bench To Understanding

Modeling Disease
In A Dish

Patient-derived stem cells let us watch HGPS unfold outside the body — and test what reverses it.

Meet the Team
Dr. Kan Cao, Principal Investigator

Welcome!

Understanding a rare disease to understand us all.

Hutchinson–Gilford Progeria Syndrome compresses many hallmarks of aging into childhood. By integrating stem cell biology, engineering, artificial intelligence, and machine learning, we investigate how aging unfolds at the cellular and molecular levels. These interdisciplinary approaches help us build a deeper understanding of the aging process we all experience, uncover mechanisms underlying age-related neurological diseases such as Alzheimer’s disease, and develop innovative strategies to improve human health and healthy longevity.

We also translate discoveries in aging biology into real-world applications. One example is how our skin-aging research has been translated into innovative skincare products through Mblue Labs and Bluelene®.

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How We're Studying It

Three connected threads of research, each looking at aging from a different angle.

Aging

Progeria · Alzheimer's Disease · Cellular Aging

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Resilience

Mitochondria · Bioenergetics · Stress Response

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Regeneration

Wound Healing · Laminopathies · Therapeutics

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Researcher examining a sample under a microscope

One Gene. Two Timelines.

HGPS arises from a single mutation in the LMNA gene, producing a toxic protein fragment called progerin. In children who carry it, many hallmarks of old age appear within a matter of years — giving us a rare, sharpened window into the much slower process every one of us goes through.

Meet the Team

Sharing the Knowledge

Building Insights

Identifying which genomic regions shift under progerin's influence, and how those changes ripple outward.

Breaking Boundaries

Reprogramming patient cells into iPSCs to watch the disease unfold outside the body, in real time.

Implementing Ideas

Testing whether the same mechanisms drive normal aging, just slower and quieter.

University of Maryland CBMG NIH NHGRI