Paul H. Kim, Ph.D. · Aging & Cell Biology
I investigate how failures in nuclear architecture drive cellular and vascular aging—using progeria as a powerful window into the biology of time.
Research focus
My work crosses scales—from nanometer-scale protein networks to the progressive loss of cells in the arterial wall.
Nuclear architecture
The nucleus is wrapped in a protein meshwork that protects DNA and helps cells withstand stress. I study how progerin distorts this scaffold, creating weak points that can rupture.
High-resolution and live-cell imaging reveal how progerin reorganizes lamin A and lamin B1 meshworks, drives nuclear membrane blebs and ruptures, and perturbs nuclear mechanics.
Vascular aging
In progeria, the smooth muscle cells that reinforce arteries are progressively lost. I investigate why these cells fail and what their vulnerability can teach us about cardiovascular aging.
Patient-derived cells, mouse models, iPSC systems, tissue microdissection, and multi-omics connect progerin accumulation and mechanical stress to smooth-muscle-cell death and arterial pathology.
Intervention science
Understanding a failure is only the beginning. I build models and assays that let research teams test potential interventions and decide what is worth advancing.
My work spans genetic and pharmacological perturbation, phenotypic screening, disease-model development, quantitative imaging, and orthogonal mechanism-of-action assays.
“Why do our cells age—and can we reverse it?”
The question guiding my researchSelected publications
Connected progressive progerin accumulation in the aorta to the selective loss of the smooth muscle cells that protect arterial structure.
Revealed large, irregular openings in the progerin meshwork and showed that higher lamin B1 expression can normalize its structure and reduce nuclear rupture.
Linked repetitive nuclear membrane rupture, mechanical stress, DNA damage, and smooth-muscle-cell death in progeria.
Showed that reducing force transmission to the nucleus protects smooth muscle cells and ameliorates arterial disease.
Featured journal covers
Visual stories from my work on nuclear mechanics, smooth muscle cell injury, and the vascular biology of premature aging.
Cover featureVolume 6 · Issue 16
Nuclear membrane ruptures underlie the vascular pathology in a mouse model of Hutchinson-Gilford progeria syndrome
Aortic smooth muscle from a progeria model mouse: nuclear tdTomato in red, elastic fibers in green, and nuclei in blue.
View the issue
Cover featureVolume 10 · Issue 460
Disrupting the LINC complex in smooth muscle cells reduces aortic disease in a mouse model of Hutchinson-Gilford progeria syndrome
A colorized transmission electron micrograph of an aortic smooth muscle cell from a mouse model of progeria.
View the issueCover images courtesy of JCI Insight and AAAS / Science Translational Medicine.
About Paul
I am a bioengineer and cell biologist interested in the mechanisms that make cells—and ultimately tissues—age.
Over a 16-year research career spanning national laboratory, academic, and industry settings, I have built disease models, imaging workflows, multi-omics studies, and functional assays that turn complex biology into measurable evidence.
My work on Hutchinson-Gilford progeria syndrome has focused on the nuclear lamina, nuclear membrane rupture, vascular smooth muscle cell loss, and the search for interventions that can protect cellular function.
DuPont · Nemours · UCLA · Sandia National Laboratories
University of California, Los Angeles
University of California, Los Angeles
College of William & Mary
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