Accelerated aging diseases comprise a group of very rare syndromes characterized by the premature development of aging-like clinical signs, Hutchinson-Gilford progeria syndrome (HGPS) and Werner syndrome (WS) being the best-known examples of this group of disorders. The main causes of the accelerated aging phenotype include defects in the nuclear envelope proteins and alterations in the DNA repair machinery. As these disorders recapitulate several hallmarks of aging, they have generated great interest in the research community because of their potential as models to explore both pathological and physiological aging.

Studying the molecular and cellular mechanisms involved in premature aging syndromes is useful not only to find therapeutic options for these disorders but also to broaden the understanding of physiological aging. Hence, over the last years, research in this field has significantly grown and different animal models have been developed to explore these syndromes. As a result, several intervention strategies have been proposed, ranging from
gene-editing approaches to systemic interventions. However, further efforts are needed to better understand the aging process, and to develop new and safe therapeutic strategies for treating progeria. At the same time, it is important to understand whether those strategies
may also impact physiological aging.

Both review and research articles are encouraged to be submitted to this Research Topic. The specific themes we would like contributors to address are, but not limited to:

• Molecular and cellular mechanisms involved in accelerated aging diseases
• New intervention strategies in progeria
• Common characteristics between premature aging syndromes and physiological aging
• Animal and cellular models for the study of progeria
• Clinical characteristics of accelerated aging syndromes and patient care
• New progeria-like syndromes

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Frontiers in Aging

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