Prelamin A Acts to Accelerate Smooth Muscle Cell Senescence and Is a Novel Biomarker of Human Vascular Aging | Zendy

Cassandra D. Ragnauth | Zendy; Derek Warren | Zendy; Yiwen Liu | Zendy; Rosamund McNair | Zendy; Tamara Tajsic | Zendy; Nichola Figg | Zendy; Rukshana Shroff | Zendy; Jeremy N. Skepper | Zendy; Catherine M. Shanahan | Zendy

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Prelamin A Acts to Accelerate Smooth Muscle Cell Senescence and Is a Novel Biomarker of Human Vascular Aging

Author(s) -

Cassandra D. Ragnauth,

Derek Warren,

Yiwen Liu,

Rosamund McNair,

Tamara Tajsic,

Nichola Figg,

Rukshana Shroff,

Jeremy N. Skepper,

Catherine M. Shanahan

Publication year - 2010

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.109.902056

Subject(s) - senescence , medicine , biomarker , vascular smooth muscle , microbiology and biotechnology , cellular senescence , cell , smooth muscle , cancer research , biochemistry , phenotype , biology , gene

Hutchinson-Gilford progeria syndrome is a rare inherited disorder of premature aging caused by mutations in LMNA or Zmpste24 that disrupt nuclear lamin A processing, leading to the accumulation of prelamin A. Patients develop severe premature arteriosclerosis characterized by vascular smooth muscle cell (VSMC) calcification and attrition.

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