Progeria causes

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vamsikrishna Gunnam M.B.B.S [2]

Overview

The most common cause of Hutchinson-Gilford progeria syndrome (HGPS) is mutation in LMNA gene.

Causes

Common Causes

Common causes of Hutchinson-Gilford progeria syndrome (HGPS) may include:[1][2][3][4]

Less Common Causes

Less common causes of Hutchinson-Gilford progeria syndrome (HGPS) include:

Genetic Causes

Causes by Organ System

Environmental No underlying causes
Gastroenterologic No underlying causes
Genetic Mutation in LMNA gene
Hematologic No underlying causes
Iatrogenic No underlying causes
Infectious Disease No underlying causes
Musculoskeletal/Orthopedic No underlying causes
Neurologic No underlying causes
Nutritional/Metabolic No underlying causes
Obstetric/Gynecologic No underlying causes
Oncologic LMNA gene mutation
Ophthalmologic No underlying causes
Overdose/Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary No underlying causes
Renal/Electrolyte No underlying causes
Rheumatology/Immunology/Allergy No underlying causes
Sexual No underlying causes
Trauma No underlying causes
Urologic No underlying causes
Miscellaneous No underlying causes

References

  1. Elzeneini E, Wickström SA (2017). "Lipodystrophic laminopathy: Lamin A mutation relaxes chromatin architecture to impair adipogenesis". J Cell Biol. 216 (9): 2607–2610. doi:10.1083/jcb.201707090. PMC 5584192. PMID 28811278.
  2. Guénantin AC, Briand N, Bidault G, Afonso P, Béréziat V, Vatier C; et al. (2014). "Nuclear envelope-related lipodystrophies". Semin Cell Dev Biol. 29: 148–57. doi:10.1016/j.semcdb.2013.12.015. PMID 24384368.
  3. Oldenburg A, Briand N, Sørensen AL, Cahyani I, Shah A, Moskaug JØ; et al. (2017). "A lipodystrophy-causing lamin A mutant alters conformation and epigenetic regulation of the anti-adipogenic MIR335 locus". J Cell Biol. 216 (9): 2731–2743. doi:10.1083/jcb.201701043. PMC 5584164. PMID 28751304.
  4. Camozzi D, Capanni C, Cenni V, Mattioli E, Columbaro M, Squarzoni S; et al. (2014). "Diverse lamin-dependent mechanisms interact to control chromatin dynamics. Focus on laminopathies". Nucleus. 5 (5): 427–40. doi:10.4161/nucl.36289. PMC 4164485. PMID 25482195.
  5. De Sandre-Giovannoli A, Lévy N (2006). "Altered splicing in prelamin A-associated premature aging phenotypes". Prog Mol Subcell Biol. 44: 199–232. PMID 17076270.