Impaired intestinal cell proliferation parallels increased senescence after burn injury in aged mice.

Travis M Walrath, Mara R Evans, Kenneth Meza Monge, Kevin M Najarro, David J Orlicky, Juan-Pablo Idrovo, Rachel H McMahan, Elizabeth J Kovacs

Department of Surgery, Division of GI, Trauma and Endocrine Surgery, University of Colorado, Anschutz Medical Campus, Aurora, Colorado, USA.Department of Surgery, Division of GI, Trauma and Endocrine Surgery, University of Colorado, Anschutz Medical Campus, Aurora, Colorado, USA. · pubmed

Paper

Abstract

The global population is aging, with one in six people projected to be 65 years or older by 2050. Since people aged 65 and older experience higher rates of morbidity and mortality after burn injury, there is an increased need to develop effective burn treatments in this age group. Heightened morbidity and risk of mortality may stem from increased gut leakiness and death of intestinal epithelial cells of aged individuals. Herein, we used our clinically relevant model of scald burn injury in young and aged mice to ascertain whether the colon, isolated colonic epithelium, and organoids grown from the colon, have deficiencies in cell growth, senescence, and apoptosis pathways. Aged, burn-injured mice displayed increased senescence marker

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Research summary

The paper claims that aged, burn-injured mice exhibit increased senescence and impaired intestinal cell proliferation. This research is relevant as it investigates the underlying mechanisms of aging-related responses to injury, which could inform strategies for improving health outcomes in the elderly.

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