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The Journal of Experimental Biology 205, 2957-2962 (2002)
© 2002 The Company of Biologists Limited

Commentary

Adaptive mechanisms of intracellular calcium homeostasis in mammalian hibernators

Shi Qiang Wang^1,2,*, Edward G. Lakatta², Heping Cheng² and Zeng Quan Zhou¹

¹ National Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing 100871, China
² Laboratory of Cardiovascular Sciences, National Institute on Aging, NIH, Baltimore, MD 21224, USA

^* Author for correspondence (e-mail: wangsq{at}grc.nia.nih.gov)

Accepted 1 July 2002

Intracellular Ca²⁺ homeostasis is a prerequisite for a healthy cell life. While cells from some mammals may suffer dysregulation of intracellular Ca²⁺ levels under certain deleterious and stressful conditions, including hypothermia and ischemia, cells from mammalian hibernators exhibit a remarkable ability to maintain a homeostatic intracellular Ca²⁺ environment. Compared with cells from non-hibernators, hibernator cells are characterized by downregulation of the activity of Ca²⁺ channels in the cell membrane, which helps to prevent excessive Ca²⁺ entry. Concomitantly, sequestration of Ca²⁺ by intracellular Ca²⁺ stores, especially the sarcoplasmic/endoplasmic reticulum, is enhanced to keep the resting levels of intracellular Ca²⁺ stable. An increase in stored Ca²⁺ in heart cells during hibernation ensures that the levels of Ca²⁺ messenger are sufficient for forceful cell contraction under conditions of hypothermia. Maintenance of Na⁺ gradients, via Na⁺—Ca²⁺ exchangers, is also important in the Ca²⁺ homeostasis of hibernator cells. Understanding the adaptive mechanisms of Ca²⁺ regulation in hibernating mammals may suggest new strategies to protect nonhibernator cells, including those of humans, from Ca²⁺-induced dysfunction.

Key words: hibernation, Ca²⁺ metabolism, adaptation, excitation—contraction coupling, homeostasis

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