Progerin and Early Vascular Aging in CKD | GeneTex

This research highlights how somatic genetic changes, specifically mosaic progerin expression, contribute to vascular pathology and increased cardiovascular disease (CVD) risk in CKD patients.

Key Findings: Progerin and Early Vascular Aging in CKD

• Somatic Progerin Expression in CKD: The study identifies recurrent somatic expression of progerin—a truncated lamin A isoform linked to Hutchinson–Gilford progeria syndrome (HGPS)—in vascular smooth muscle cells (VSMCs) of CKD arteries.
• Frequent LMNA Mutation: The classic HGPS mutation (LMNA c.1824C>T) was detected as a somatic variant in 78.3% of CKD artery samples.
• Pathological Effects: Progerin-positive VSMCs showed clonal expansion, increased DNA damage response, endoplasmic reticulum stress, and cellular senescence.
• In Vivo Evidence: Inducible lineage-tracing mouse models demonstrated that progerin-expressing VSMCs can drive EVA-like changes, including VSMC loss, medial fibrosis, and upregulation of osteogenic genes.

These findings suggest that somatic LMNA mutations and progerin expression play a significant role in early vascular aging in CKD, emphasizing the importance of investigating somatic genetic variation in common diseases.

GeneTex Antibodies Used in Nature Aging CKD Study

GeneTex’s highly cited ATR (phospho Thr1989) antibody (GTX128145) was used as a marker for DNA damage in both ICC/IF and IHC analyses of CKD vascular samples in this Nature Aging study. GeneTex supports CKD and cell biology research with a comprehensive range of validated antibodies.

Featured GeneTex Antibodies for CKD and EVA Research

ATM (phospho Ser1981) antibody [HL1062] (GTX636086)

Chk1 (phospho Ser345) antibody [HL122] (GTX635572)

p21 Cip1 antibody [GT1032] (GTX629543)

AKT1 antibody [HL1145] (GTX636416)

Explore more GeneTex products in our webshop or contact one of our account managers for more information on the antibodies for CKD, EVA, and DNA damage research.

Reference

Revêchon et al., Nat Aging. 2025 Jun;5(6):1046-1062. doi: 10.1038/s43587-025-00882-6.