{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,18]],"date-time":"2025-12-18T05:36:17Z","timestamp":1766036177518,"version":"3.48.0"},"reference-count":93,"publisher":"MDPI AG","issue":"4","license":[{"start":{"date-parts":[[2025,12,15]],"date-time":"2025-12-15T00:00:00Z","timestamp":1765756800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Koltzov Institute of Developmental Biology of the Russian Academy of Sciences","award":["0088-2024-0013"],"award-info":[{"award-number":["0088-2024-0013"]}]},{"DOI":"10.13039\/501100006769","name":"Russian Science Foundation","doi-asserted-by":"crossref","award":["21-74-30015-\u041f"],"award-info":[{"award-number":["21-74-30015-\u041f"]}],"id":[{"id":"10.13039\/501100006769","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Medical Sciences"],"abstract":"<jats:p>Children with Hutchinson\u2013Gilford progeria syndrome (HGPS) are born without height and weight abnormalities, and postnatal development is delayed from two months of age. The pathophysiological manifestations of HGPS can be categorized into the three tissue systems that are primarily affected: bone and cartilage, the smooth muscular layer of the vasculature, and the dermis layer. To understand the biology of the syndrome\u2019s complications resulting from the inherited dominant mutation of the LMNA gene, HGPS has to be considered in embryogenesis. Since the development of the primarily affected HGPS tissues involves a simultaneous contribution of mesodermal and neural crest cells, we hypothesized that the stochastic and heterogeneous coexistence of mesoderm and neural crest cells might be crucial for the onset and manifestation of HGPS. In addition, the expression of Lamin A and\/or progerin during embryonic development tends to accumulate in the cell nucleus, causing the syndrome manifestation. Then, how and why are infants with the LMNA gene mutation born without severe deviations? Migration is a distinguishing property of mesoderm and neural crest cells, so that they are continuously subjected to mechanical stimuli throughout development and require normal lamina function. However, the viscoelastic property and the mechanosensor capability to respond to mechanical stress of the HGPS cell nucleus are disturbed. Despite the presence of progerin in development, we assume that high levels of Lamin B1 in cells determine the delayed onset of HGPS after birth. We also hypothesized that progerin toxicity could be managed and prevented, potentially allowing for rescue by the presence of Lamin B1.<\/jats:p>","DOI":"10.3390\/medsci13040321","type":"journal-article","created":{"date-parts":[[2025,12,15]],"date-time":"2025-12-15T15:15:08Z","timestamp":1765811708000},"page":"321","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Why and How Are Infants with Hutchinson\u2013Gilford Progeria Syndrome Born Without Severe Manifestations?"],"prefix":"10.3390","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-7613-3282","authenticated-orcid":false,"given":"Mariia A.","family":"Erokhina","sequence":"first","affiliation":[{"name":"Institute of Gene Biology, Russian Academy of Sciences, Vavilov Str. 34\/5, 119334 Moscow, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5405-0212","authenticated-orcid":false,"given":"Ekaterina A.","family":"Vorotelyak","sequence":"additional","affiliation":[{"name":"Laboratory of Cell Biology, N.K. Koltzov Institute of Developmental Biology, Russian Academy of Sciences, Vavilov Str. 26, 119334 Moscow, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrey V.","family":"Vasiliev","sequence":"additional","affiliation":[{"name":"Laboratory of Cell Biology, N.K. Koltzov Institute of Developmental Biology, Russian Academy of Sciences, Vavilov Str. 26, 119334 Moscow, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5697-3774","authenticated-orcid":false,"given":"Vepa K.","family":"Abdyev","sequence":"additional","affiliation":[{"name":"Laboratory of Cell Biology, N.K. Koltzov Institute of Developmental Biology, Russian Academy of Sciences, Vavilov Str. 26, 119334 Moscow, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2025,12,15]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"592","DOI":"10.1056\/NEJMoa0706898","article-title":"Phenotype and course of Hutchinson-Gilford progeria syndrome","volume":"358","author":"Merideth","year":"2008","journal-title":"N. Engl. J. Med."},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"249","DOI":"10.1016\/B978-0-444-62702-5.00018-4","article-title":"Hutchinson-Gilford progeria syndrome","volume":"132","author":"Ullrich","year":"2015","journal-title":"Handb. Clin. 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