Author
Susan V. Brooks
University of MichiganORCID 0000-0003-1954-967XUnclaimed ORCID profile · follow to get notified of new preprints
Biology Disciplines
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2024-2026 · peak 3/yrCo-Author Collaboration Network
10 top collaborators · 26 mutual co-author links6 papers
Recent·Most cited
- PhysiologyFEBS JournalPeer-reviewed12 citations
- PathologyJCI InsightPeer-reviewed
Histopathology and spatial transcriptomics jointly map myofiber-specific pathological programs in mTORC1-driven myopathy
Jer-En Hsu, Qingyang Zhao, Weiqiu Cheng…·Jun Hee Lee
This study combines histopathology and spatial transcriptomics to show that mTORC1 hyperactivation causes fiber-type-specific pathological changes in skeletal muscle.
DOI 10.1172/jci.insight.203167 - NeuroscienceJCI InsightPeer-reviewed
Decoding muscle-resident Schwann cell dynamics during neuromuscular junction remodeling
Steve D. Guzman, Ahmad Abu-Mahfouz, Carol S. Davis…·Susan V. Brooks
This study uses scRNA-Seq to analyze Schwann cell subtypes during NMJ remodeling, identifying a novel tSC subtype and SPP1 signaling's role in reinnervation.
- Developmental BiologyMolecular MetabolismPeer-reviewed
Leukocyte-type 12/15-lipoxygenase is essential for timely inflammation-resolution and effective tissue regeneration following skeletal muscle injury
Binayok Sharma, Xinyue Lu, Hafeez-u- Rehman…·James F. Markworth
This study shows that 12/15-LOX is essential for inflammation resolution and skeletal muscle regeneration by regulating lipid mediators and myogenic progenitor cell function.
14 citationstop 1% - PathologybioRxivPreprint
AMP-activated protein kinase (AMPK) is essential for tendon homeostasis and prevents premature senescence and ectopic calcification
LeeAnn A. Hold, Nicole Migotsky, Syeda N. Lamia…·Adam C. Abraham
This study shows AMPK1 is essential for tendon health, preventing senescence and calcification through metabolic regulation and ECM remodeling.
DOI 10.1101/2025.01.31.635920 - PhysiologyThe FASEB JournalPeer-reviewed
Overexpression of enhanced yellow fluorescent protein fused with Channelrhodopsin-2 causes contractile dysfunction in skeletal muscle
Syeda N. Lamia, Carol S. Davis, Peter C. D. Macpherson…·Megan Leigh Killian
This study shows that overexpressing ChR2-EYFP in skeletal muscle causes contractile dysfunction, while ChR2-only mice show normal function, highlighting the need for alternative optogenetic models.
2 citations