ER stress in cardiac aging, a current view on the D-galactose model

Longitudinal studies are mandatory to study aging, however, they have certain drawbacks, for example, they require strict maintenance that is expensive given the breeding time (approximately 2 years) and with a low survival rate, having some animals to study very limitedly. In vitro studies provide useful and invaluable in-formation on the cellular and molecular mechanisms that help understand the aging process to overcome these aspects. In particular, the model of premature aging induced by chronic exposure to D-galactose (D-Gal) offers a very similar picture to that which occurs in natural aging. This model mimics most of the old animals' cellular processes, such as oxidative stress, mitochondrial dysfunction, increased advanced glycation end products (AGEs), inflammation, and senescence-associated secretory phenotype (SASP). However, the information related to the endoplasmic reticulum (ER) stress and, subsequently, the unfolded protein response (UPR) is not fully elucidated. Therefore, this review brings together the most current information on this response in the D-Gal -induced aging model and its effect on cardiac structure and function.

Automated summary

Longitudinal studies are necessary to study aging, but they have limitations. In vitro studies provide valuable information on understanding the aging process. The D-galactose-induced premature aging model mimics many cellular processes seen in natural aging, but the role of endoplasmic reticulum stress and unfolded protein response is not fully understood.