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The structure and function of lamin A/C: Special focus on cardiomyopathy and therapeutic interventions.
Tiwari, Vikas; Alam, Md Jahangir; Bhatia, Madhavi; Navya, Malladi; Banerjee, Sanjay K.
Afiliación
  • Tiwari V; Department of Biotechnology, National Institute of Pharmaceutical Education and Research, Guwahati 781101, Assam, India.
  • Alam MJ; Department of Biotechnology, National Institute of Pharmaceutical Education and Research, Guwahati 781101, Assam, India; Cell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
  • Bhatia M; Department of Biotechnology, National Institute of Pharmaceutical Education and Research, Guwahati 781101, Assam, India.
  • Navya M; Department of Biotechnology, National Institute of Pharmaceutical Education and Research, Guwahati 781101, Assam, India.
  • Banerjee SK; Department of Biotechnology, National Institute of Pharmaceutical Education and Research, Guwahati 781101, Assam, India. Electronic address: sanjay@niperguwahati.in.
Life Sci ; 341: 122489, 2024 Mar 15.
Article en En | MEDLINE | ID: mdl-38340979
ABSTRACT
Lamins are inner nuclear membrane proteins that belong to the intermediate filament family. Lamin A/C lie adjacent to the heterochromatin structure in polymer form, providing skeletal to the nucleus. Based on the localization, lamin A/C provides nuclear stability and cytoskeleton to the nucleus and modulates chromatin organization and gene expression. Besides being the structural protein making the inner nuclear membrane in polymer form, lamin A/C functions as a signalling molecule involved in gene expression as an enhancer inside the nucleus. Lamin A/C regulates various cellular pathways like autophagy and energy balance in the cytoplasm. Its expression is highly variable in differentiated tissues, higher in hard tissues like bone and muscle cells, and lower in soft tissues like the liver and brain. In muscle cells, including the heart, lamin A/C must be expressed in a balanced state. Lamin A/C mutation is linked with various diseases, such as muscular dystrophy, lipodystrophy, and cardiomyopathies. It has been observed that a good number of mutations in the LMNA gene impact cardiac activity and its function. Although several works have been published, there are still several unexplored areas left regarding the lamin A/C function and structure in the cardiovascular system and its pathological state. In this review, we focus on the structural organization, expression pattern, and function of lamin A/C, its interacting partners, and the pathophysiology associated with mutations in the lamin A/C gene, with special emphasis on cardiovascular diseases. With the recent finding on lamin A/C, we have summarized the possible therapeutic interventions to treat cardiovascular symptoms and reverse the molecular changes.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Distrofias Musculares / Cardiomiopatías Límite: Humans Idioma: En Revista: Life Sci Año: 2024 Tipo del documento: Article País de afiliación: India Pais de publicación: Países Bajos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Distrofias Musculares / Cardiomiopatías Límite: Humans Idioma: En Revista: Life Sci Año: 2024 Tipo del documento: Article País de afiliación: India Pais de publicación: Países Bajos