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. 2017 Aug 4;8:575. doi: 10.3389/fphys.2017.00575

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Copyright © 2017 Seebacher and Little.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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A summary of the potential mechanisms underlying cell-autonomous thermal plasticity. Transient receptor potential channels vanilloid 4 (TRPV4) and melastatin 8 (TRPM8) upregulate expression of peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α) and uncoupling protein 1 (UCP1), respectively, in response to local hypothermia (blue arrows; normothermic conditions depicted by red arrows). Cold-inducible RNA binding protein (CIRBP) expression is enhanced in response to cold exposure through a temperature-sensitive change in RNA splicing that determines the proportion pre-mRNA processed into mature mRNA. Relative translation rates for RNA binding motif protein 3 (RBM3) is enhanced during cold exposure via a 5' internal ribosome entry site (IRES), while global protein synthesis declines. AMP-activated protein kinase (AMPK) is activated by increasing ratio of AMP:ATP with cold exposure, thereby enhancing PGC1α activity.