Control of adipocyte senescence

Casadio, Melina

doi:10.1038/s41556-022-00922-y

Cited by 1 publication

(1 citation statement)

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“…Furthermore, upregulation of p53 in adipocytes and macrophages promoted senescence and increased insulin resistance and inflammatory cytokines in mice ( 45 ). Most senescent cells have been found in white adipose tissues (WAT) ( 46 – 48 ). Transplantation studies of WAT from progeria or obese mouse models caused insulin resistance in host/recipient mice, demonstrating that senescent cells from fat are responsible, in part, to the onset of diabetes ( 45 ).…”

Section: Cellular Senescence In Diabetesmentioning

confidence: 99%

Reversing and modulating cellular senescence in beta cells, a new field of opportunities to treat diabetes

Rubin de Celis,

Bonner-Weir

2023

Front. Endocrinol.

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Diabetes constitutes a world-wide pandemic that requires searching for new treatments to halt its progression. Cellular senescence of pancreatic beta cells has been described as a major contributor to development and worsening of diabetes. The concept of reversibility of cellular senescence is critical as is the timing to take actions against this “dormant” senescent state. The reversal of cellular senescence can be considered as rejuvenation of the specific cell if it returns to the original “healthy state” and doesn’t behave aberrantly as seen in some cancer cells. In rodents, treatment with senolytics and senomorphics blunted or prevented disease progression, however their use carry drawbacks. Modulators of cellular senescence is a new area of research that seeks to reverse the senescence. More research in each of these modalities should lead to new treatments to stop diabetes development and progression.

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