Myocardial infarction augments sleep to limit cardiac inflammation and damage

Pacific Huynh, Jan D. Hoffmann, Teresa Gerhardt, Máté G. Kiss, Faris M. Zuraikat, Oren Cohen, Christopher Wolfram, Abi G. Yates, Alexander Leunig, Merlin Heiser, Lena Gaebel, Matteo Gianeselli, Sukanya Goswami, Annie Khamhoung, Jeffrey Downey, Seonghun Yoon, Zhihong Chen, Vladimir Roudko, Travis Dawson, Joana Ferreira da Silva, Natalie J. Ameral, Jarod Morgenroth-Rebin, Darwin D’Souza, Laura L. Koekkoek, Walter Jacob, Jazz Munitz, Donghoon Lee, John F. Fullard, Mandy M. T. Leent, Panos Roussos, Seunghee Kim-Schulze, Neomi Shah, Benjamin P. Kleinstiver, Filip K. Swirski, David Leistner, Marie-Pierre St-Onge and Cameron S. McAlpine ()
Additional contact information
Pacific Huynh: Icahn School of Medicine at Mount Sinai
Jan D. Hoffmann: Icahn School of Medicine at Mount Sinai
Teresa Gerhardt: Icahn School of Medicine at Mount Sinai
Máté G. Kiss: Icahn School of Medicine at Mount Sinai
Faris M. Zuraikat: Columbia University Irving Medical Center
Oren Cohen: Icahn School of Medicine at Mount Sinai
Christopher Wolfram: Germany and Berlin Institute of Health
Abi G. Yates: Icahn School of Medicine at Mount Sinai
Alexander Leunig: Icahn School of Medicine at Mount Sinai
Merlin Heiser: Icahn School of Medicine at Mount Sinai
Lena Gaebel: Icahn School of Medicine at Mount Sinai
Matteo Gianeselli: Icahn School of Medicine at Mount Sinai
Sukanya Goswami: Icahn School of Medicine at Mount Sinai
Annie Khamhoung: Icahn School of Medicine at Mount Sinai
Jeffrey Downey: Icahn School of Medicine at Mount Sinai
Seonghun Yoon: Icahn School of Medicine at Mount Sinai
Zhihong Chen: Icahn School of Medicine at Mount Sinai
Vladimir Roudko: Icahn School of Medicine at Mount Sinai
Travis Dawson: Icahn School of Medicine at Mount Sinai
Joana Ferreira da Silva: Massachusetts General Hospital
Natalie J. Ameral: Harvard Medical School
Jarod Morgenroth-Rebin: Massachusetts General Hospital
Darwin D’Souza: Icahn School of Medicine at Mount Sinai
Laura L. Koekkoek: Icahn School of Medicine at Mount Sinai
Walter Jacob: Icahn School of Medicine at Mount Sinai
Jazz Munitz: Icahn School of Medicine at Mount Sinai
Donghoon Lee: Icahn School of Medicine at Mount Sinai
John F. Fullard: Icahn School of Medicine at Mount Sinai
Mandy M. T. Leent: Icahn School of Medicine at Mount Sinai
Panos Roussos: Icahn School of Medicine at Mount Sinai
Seunghee Kim-Schulze: Icahn School of Medicine at Mount Sinai
Neomi Shah: Icahn School of Medicine at Mount Sinai
Benjamin P. Kleinstiver: Massachusetts General Hospital
Filip K. Swirski: Icahn School of Medicine at Mount Sinai
David Leistner: Germany and Berlin Institute of Health
Marie-Pierre St-Onge: Columbia University Irving Medical Center
Cameron S. McAlpine: Icahn School of Medicine at Mount Sinai

Nature, 2024, vol. 635, issue 8037, 168-177

Abstract: Abstract Sleep is integral to cardiovascular health1,2. Yet, the circuits that connect cardiovascular pathology and sleep are incompletely understood. It remains unclear whether cardiac injury influences sleep and whether sleep-mediated neural outputs contribute to heart healing and inflammation. Here we report that in humans and mice, monocytes are actively recruited to the brain after myocardial infarction (MI) to augment sleep, which suppresses sympathetic outflow to the heart, limiting inflammation and promoting healing. After MI, microglia rapidly recruit circulating monocytes to the brain’s thalamic lateral posterior nucleus (LPN) via the choroid plexus, where they are reprogrammed to generate tumour necrosis factor (TNF). In the thalamic LPN, monocytic TNF engages Tnfrsf1a-expressing glutamatergic neurons to increase slow wave sleep pressure and abundance. Disrupting sleep after MI worsens cardiac function, decreases heart rate variability and causes spontaneous ventricular tachycardia. After MI, disrupting or curtailing sleep by manipulating glutamatergic TNF signalling in the thalamic LPN increases cardiac sympathetic input which signals through the β2-adrenergic receptor of macrophages to promote a chemotactic signature that increases monocyte influx. Poor sleep in the weeks following acute coronary syndrome increases susceptibility to secondary cardiovascular events and reduces the heart’s functional recovery. In parallel, insufficient sleep in humans reprogrammes β2-adrenergic receptor-expressing monocytes towards a chemotactic phenotype, enhancing their migratory capacity. Collectively, our data uncover cardiogenic regulation of sleep after heart injury, which restricts cardiac sympathetic input, limiting inflammation and damage.

Date: 2024
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DOI: 10.1038/s41586-024-08100-w

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