Endoplasmic reticulum stress, calcium homeostasis and the aging heart.

Izabela Quest, Marek Michalak

University of Alberta, Department of Biochemistry, Edmonton, Alberta, Canada; [email protected] of Alberta, Department of Biochemistry, Edmonton, Alberta, Canada; [email protected]. · pubmed

Paper

Abstract

Aging is a process characterized by the progressive decline in physiological function and increased susceptibility to disease. Many cellular functions, including unfolded protein responses (UPR, an endoplasmic reticulum (ER) stress coping mechanism), Ca2+ signaling, cellular signaling and inflammatory responses are affected by aging. These significantly impact Ca2+ handling by cardiac cells and the architecture of cardiomyocytes, leading to impaired contractility, and increased risk of arrhythmias. Cellular Ca2+ homeostasis and the UPR are interdependent, therefore, understanding and influencing these key cellular pathways should provide new therapeutic strategies for managing age-related cardiac diseases. Modulating Ca2+ handling and cellular stress pathways presents distinctive approaches to preventing molecular alterations linked to aging, while providing opportunities to reduce molecular damage and promote the effectiveness of cellular repair processes.

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Research summary

Modulating Ca2+ handling and cellular stress pathways can provide new therapeutic strategies for managing age-related cardiac diseases. The paper addresses fundamental cellular mechanisms that contribute to aging and age-related diseases, focusing on potential interventions that target the root causes of these conditions.

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