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BUFFALO, NY — September 29, 2026 — A new #review was #published in Volume 18 of Aging on September 8, 2026, titled “Developmental senescence misregulation in congenital disorders: CHARGE syndrome as a candidate model.”
The article proposes that disruption of developmental senescence—a tightly controlled cellular program involved in embryonic tissue remodeling—may contribute to congenital abnormalities associated with CHARGE syndrome.
The review was led by co-first authors Álvaro J. Arana and Pablo Palau-Irisarri, who contributed equally. Arana is affiliated with the Departamento de Zoología, Genética y Antropología Física, Facultad de Veterinaria, Universidad de Santiago de Compostela, Spain, while Palau-Irisarri is affiliated with the Departamento de Biología, Facultad de Ciencias, Universidad Autónoma de Madrid, Spain. Arana is also the corresponding author.
Cellular senescence is commonly associated with aging, cellular stress and tumor suppression, but it also occurs naturally during embryonic development. Unlike classical stress-induced senescence, developmental senescence is transient and restricted to particular tissues and developmental stages. These cells can contribute to tissue remodeling and patterning before being cleared, helping shape developing organs.
Because this process must occur at the right place and time, the authors propose that excessive, insufficient, prolonged or misplaced senescence could interfere with normal morphogenesis. CHARGE syndrome provides a particularly relevant model for investigating this possibility. The rare developmental disorder can involve coloboma, heart defects, choanal atresia, growth and developmental delay, genitourinary abnormalities and characteristic ear defects. Most patients with CHARGE syndrome carry pathogenic variants in CHD7, which encodes an ATP-dependent chromatin remodeler.
Full press release - https://www.aging-us.com/news-room/developmental-senescence-emerges-as-a-candidate-mechanism-in-charge-syndrome
DOI - https://doi.org/10.18632/aging.206396
Corresponding author - Álvaro J. Arana - alvaro.arana@usc.es
Abstract video - https://www.youtube.com/watch?v=QtB5390b1To
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Keywords - aging, CHD7, morphogenesis, p53/p21 pathway, TGFβ signaling, congenital disorders
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The article proposes that disruption of developmental senescence—a tightly controlled cellular program involved in embryonic tissue remodeling—may contribute to congenital abnormalities associated with CHARGE syndrome.
The review was led by co-first authors Álvaro J. Arana and Pablo Palau-Irisarri, who contributed equally. Arana is affiliated with the Departamento de Zoología, Genética y Antropología Física, Facultad de Veterinaria, Universidad de Santiago de Compostela, Spain, while Palau-Irisarri is affiliated with the Departamento de Biología, Facultad de Ciencias, Universidad Autónoma de Madrid, Spain. Arana is also the corresponding author.
Cellular senescence is commonly associated with aging, cellular stress and tumor suppression, but it also occurs naturally during embryonic development. Unlike classical stress-induced senescence, developmental senescence is transient and restricted to particular tissues and developmental stages. These cells can contribute to tissue remodeling and patterning before being cleared, helping shape developing organs.
Because this process must occur at the right place and time, the authors propose that excessive, insufficient, prolonged or misplaced senescence could interfere with normal morphogenesis. CHARGE syndrome provides a particularly relevant model for investigating this possibility. The rare developmental disorder can involve coloboma, heart defects, choanal atresia, growth and developmental delay, genitourinary abnormalities and characteristic ear defects. Most patients with CHARGE syndrome carry pathogenic variants in CHD7, which encodes an ATP-dependent chromatin remodeler.
Full press release - https://www.aging-us.com/news-room/developmental-senescence-emerges-as-a-candidate-mechanism-in-charge-syndrome
DOI - https://doi.org/10.18632/aging.206396
Corresponding author - Álvaro J. Arana - alvaro.arana@usc.es
Abstract video - https://www.youtube.com/watch?v=QtB5390b1To
Sign up for free Altmetric alerts about this article -
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206396
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
Keywords - aging, CHD7, morphogenesis, p53/p21 pathway, TGFβ signaling, congenital disorders
To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:
Bluesky - https://bsky.app/profile/aging-us.bsky.social
ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589
X - https://twitter.com/AgingJrnl
Facebook - https://www.facebook.com/AgingUS/
Instagram - https://www.instagram.com/agingjrnl/
LinkedIn - https://www.linkedin.com/company/aging/
Reddit - https://www.reddit.com/user/AgingUS/
Pinterest - https://www.pinterest.com/AgingUS/
YouTube - https://www.youtube.com/@Aging-US
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc
MEDIA@IMPACTJOURNALS.COM
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