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Miriam Merad on Muck Rack

Miriam Merad

As seen in: AIChE Journal, Nature, The BMJ, Science Magazine, BioRxiv, Cell Host & Microbe, Cell Press, NewsBreak, NewsX, eLife
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Articles

Macrophages are constitutive architects of tissue integrity

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By Miriam Merad
| Nature Verified
The lineage distinction between inflammatory, defence-oriented, monocyte-derived macrophages and resident macrophages dedicated to tissue maintenance calls into question the primordial function of macrophages and offers untapped therapeutic targets in these cells.
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Immune aging biomarkers for clinical trials

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By Andrea Cipriano, Jamie Justice, Jesse R. Poganik, Omar O. Abudayyeh, Jonathan S. Gootenberg, Laura Haynes, Yotam Levin, Daniel E. Martin-Herranz, Arne N Akbar, Joan B. Mannick, Graham Pawelec, Shai S Shen-Orr, John S. Tsang, Wolfgang Wagner, Miriam Merad, Sacha Gnjatic, Michael Corley, George A. Kuchel, Luigi Ferrucci, David Furman, Chiara Herzog, Alfred Gellhorn
| Nature Verified
Abstract Aging profoundly remodels the immune system, impairing defense, repair and homeostatic function across tissues. Because the immune system operates in every organ, its deterioration has been proposed to drive or exacerbate systemic dysfunction and accelerate overall biological aging, making it an attractive biomarker and target for geroscience-guided trials. Despite this central role, there is no consensus on how to quantify immune aging, especially in clinical trials.
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Mutation-dependent responses to sleep and exercise in clonal haematopoiesis

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By Teresa Gerhardt, Walter Jacob, Merlin Heiser, Christopher Wolfram, Pacific Huynh, Tetsushi Nakao, Pamela Toh, Aaron Douglas, Niki F Brisnovali, Emir Radkevich, Mesbah Uddin, Abi Yates, Nader Yatim, Matteo Gianeselli, Máté G. Kiss, Sukanya Goswami, Darwin D’Souza, Zhihong Chen, Seunghee Kim-schulze, Trevor P. Fidler, Daniel Ezzat, Shaan Khurshid, Alexander Bick, Pradeep Natarajan, Patrick T. Ellinor, Abha K. Rajbhandari, Miriam Merad, Filip K. Swirski, Oren Cohen, Leigh Goedeke, Michael C. Honigberg, Cameron S. McAlpine, Lena Gaebel, Annie Khamhoung, Daniella Nelson
| Nature Verified
Abstract Clonal haematopoiesis (CH) activates inflammation and increases the risk of atherosclerosis1,2. Whether lifestyle alters CH clone expansion or the phenotypic programming of CH mutant cells, thereby affecting atherosclerosis, is unknown. Here, in humans and mice and across mutations in Jak2, Tet2, Trp53 and Dnmt3a, we demonstrate mutation-dependent responses to sleep and exercise in CH and show that mutant cells are uniquely sensitive to lifestyle.
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