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. 2022 Nov 22;119(6):1403–1415. doi: 10.1093/cvr/cvac174

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© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Proposed mechanotransduction mechanism mediating myogenic reactivity in skeletal muscle resistance arteries. Shown is the proposed molecular mechanism regulating myogenic responsiveness in skeletal muscle resistance arteries. Membrane-bound tumour necrosis factor (mTNF) and a tumour necrosis factor receptor (TNFR) form a mechanosensitive pair. Upon mechanical stimulation, both mTNF and TNFR generate signals; the signal generated by TNFR regulates a larger proportion of myogenic tone than mTNF (∼75% vs. 25%) and is not rhythmic. The mTNF signalosome incorporates CK1 as a pivotal element for the propagation of the mTNF-dependent reverse signal; the mTNF signalosome also incorporates a yet undefined element that is under circadian control. Accordingly, the mTNF reverse signal and the ∼25% of the myogenic response that it controls display circadian rhythmicity.