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J Mol Med (Berl). 2012 Dec;90(12):1361-89. doi: 10.1007/s00109-012-0962-4. Epub 2012 Oct 23.

Potential therapeutic approaches for modulating expression and accumulation of defective lamin A in laminopathies and age-related diseases.

Author information

1
Bioinformatics and Medical Information Technology Laboratory, Center for Pediatric Hematology, Oncology and Immunology, Moscow 119296, Russia. alex@biogerontology.org

Abstract

Scientific understanding of the genetic components of aging has increased in recent years, with several genes being identified as playing roles in the aging process and, potentially, longevity. In particular, genes encoding components of the nuclear lamina in eukaryotes have been increasingly well characterized, owing in part to their clinical significance in age-related diseases. This review focuses on one such gene, which encodes lamin A, a key component of the nuclear lamina. Genetic variation in this gene can give rise to lethal, early-onset diseases known as laminopathies. Here, we analyze the literature and conduct computational analyses of lamin A signaling and intracellular interactions in order to examine potential mechanisms for altering or slowing down aberrant Lamin A expression and/or for restoring the ratio of normal to aberrant lamin A. The ultimate goal of such studies is to ameliorate or combat laminopathies and related diseases of aging, and we provide a discussion of current approaches in this review.

PMID:
23090008
PMCID:
PMC3506837
DOI:
10.1007/s00109-012-0962-4
[Indexed for MEDLINE]
Free PMC Article

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