ArticleAmerican journal of physiology. Cell physiology2026
CTLA4-Ig reduces proliferation and inflammatory gene expression in muscle fibroblasts, corresponding to less fibrosis and inflammation in
Michelle Wehling-Henricks, Pranav Kannan, Connor Thomas, Harsimer Bal, Vedant Balu, Eisuke Ochi, Kenneth Dorshkind, James G Tidball
Abstract read
In one paragraphArticle in American journal of physiology. Cell physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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What it found
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2 · The registryThe trial behind it
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3 · Its place in the literatureWho cites it
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4 · The recordCorrections and comments
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5 · Who and what moneyAuthors and funding
8 authors.
Michelle Wehling-HenricksDepartment of Integrative Biology and Physiology, University of California, Los Angeles, California, United States.ORCID 0009-0000-2228-6255 Pranav KannanDepartment of Integrative Biology and Physiology, University of California, Los Angeles, California, United States.
Connor ThomasDepartment of Integrative Biology and Physiology, University of California, Los Angeles, California, United States.
Harsimer BalDepartment of Integrative Biology and Physiology, University of California, Los Angeles, California, United States.
Vedant BaluDepartment of Integrative Biology and Physiology, University of California, Los Angeles, California, United States.ORCID 0009-0005-2938-1278 Eisuke OchiFaculty of Bioscience and Applied Chemistry, Graduate School of Sports and Health Studies, Hosei University, Tokyo, Japan.
Kenneth DorshkindDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, University of California, Los Angeles, California, United States.
James G TidballDepartment of Integrative Biology and Physiology, University of California, Los Angeles, California, United States.ORCID 0000-0003-1202-8038 Funding
Myeloid-cell mediated mechanisms driving muscle growth and regenerationR01AR066036 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TIDBALL, JAMES G · 2014 to 2018
$1.8MDeveloping co-stimulatory blockade as a therapeutic strategy for Duchenne muscular dystrophyR01NS109117 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TIDBALL, JAMES G · 2019 to 2023
$1.7MImmune cell regulation of the regeneration of dystrophic muscleR01AR062579 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TIDBALL, JAMES G · 2014 to 2018
$1.7MNovel mechanisms regulating muscle growth and regeneration: elucidating the Klotho/Jmjd3/Wnt axisR01AR075768 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TIDBALL, JAMES G · 2020 to 2024
$1.7MHHS | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) RO1AR062579HHS | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) RO1AR066036HHS | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) RO1AR075768NIAMS NIH HHS R01 AR062579NIAMS NIH HHS R01 AR066036NIAMS NIH HHS R01 AR075768NINDS NIH HHS R01 NS109117
6 · The paper itselfAbstract
Muscle pathology in Duchenne muscular dystrophy (DMD) is greatly amplified by the immune response to dystrophic muscle, which provides the rationale for targeting the immune system in DMD therapies. Much of immune-driven pathology in the
Indexed as
AbataceptCell ProliferationFibroblastsInflammationMuscle, SkeletalMuscular Dystrophy, AnimalMuscular Dystrophy, DuchenneAnimalsFibrosisLymphocyte ActivationMaleMiceMice, Inbred C57BLMice, Inbred mdxAbataceptDuchenne muscular dystrophyfibrosismuscular dystrophymyositisskeletal muscle
Identifiers
PMID41855092
PMCPMC13552821
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