Key result
Repeated social defeat stress in rats impairs cardiomyocyte contractility, Ca2+ dynamics, and mitochondrial bioenergetics.
Why the study?
Chronic social stress is epidemiologically linked to increased cardiovascular disease risk, but the underlying pathophysiological mechanisms and potential mitochondrial involvement remain largely elusive.
Does repeated social defeat stress impair cardiomyocyte contractile performance and mitochondrial bioenergetics in male adult rats?
Does repeated social defeat stress impair cardiomyocyte contractile performance and mitochondrial bioenergetics in male adult rats?
Repeated social stress in male rats impairs cardiomyocyte contractile performance and alters mitochondrial bioenergetics, providing a potential pathophysiological mechanism linking social stress to cardiovascular disease.
Rodent social stress model links mitochondrial changes to cardiac mechanics; leaves open human mechanistic relevance and therapeutic translation.
Chronic social stress has been epidemiologically linked to increased risk for cardiovascular disease, yet the underlying pathophysiological mechanisms are still largely elusive. Mitochondrial (dys)function represents a potential intersection point between social stress exposure and (mal)adaptive cardiac responses. In this study, we used a rodent model of social stress to study the extent to which alterations in the cellular mechanical properties of the heart were associated with changes in indexes of mitochondrial function. Male adult rats were exposed to repeated episodes of social defeat stress or left undisturbed (controls). ECG signals were recorded during and after social defeat stress. Twenty-four hours after the last social defeat, cardiomyocytes were isolated for analyses of mechanical properties and intracellular Ca 2+ dynamics, mitochondrial respiration, and ATP content. Results indicated that social defeat stress induced potent cardiac sympathetic activation that lasted well beyond stress exposure. Moreover, cardiomyocytes of stressed rats showed poor contractile performance (e.g., slower contraction and relaxation rates) and intracellular Ca 2+ derangement (e.g., slower Ca 2+ clearing), which were associated with indexes of reduced reserve respiratory capacity and decreased ATP production. In conclusion, this study suggests that repeated social stress provokes impaired cardiomyocyte contractile performance and signs of altered mitochondrial bioenergetics in the rat heart. Future studies are needed to clarify the causal link between cardiac and mitochondrial functional remodeling under conditions of chronic social stress.
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Barbetti et al. (2022) studied Chronic social stress. Repeated episodes of social defeat stress vs. Undisturbed controls was evaluated on Cardiomyocyte mechanical properties, intracellular Ca2+ dynamics, mitochondrial respiration, and ATP content. Repeated social defeat stress in male rats provoked impaired cardiomyocyte contractile performance, intracellular Ca2+ derangement, and signs of altered mitochondrial bioenergetics.
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