Steven Welc

Assistant Professor

Indiana University School of Medicine

United States

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Steven Welc is an Assistant Professor at Indiana University School of Medicine, USA. His research focuses on muscle and bone health, specifically in relation to Duchenne Muscular Dystrophy, aging, and the mechanisms of muscle regeneration. Recent publications explore the cardioprotective role of Klotho, the effects of myeloid cells on muscle injury, and the regulation of glucose transporters in skeletal muscle.

Articles (10)

Year:

2025

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2025

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2025

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2024

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2024

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2024

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2022

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2022

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2021

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2020

Collaborators (5)

James G. Tidball

UNITED STATES

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Geoffrey D. Holman

University of Bath

UNITED KINGDOM

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Paul W Hruz

Associate Professor

Washington University Physicians

UNITED STATES

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Craig Goergen

Associate Professor

Purdue University

UNITED STATES

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E. Dale Abel

Chair/Professor

Ronald Reagan UCLA Medical Center

UNITED STATES

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Steven Welc

Research Interests

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Articles (10)

Klotho Is Cardioprotective in the mdx Mouse Model of Duchenne Muscular Dystrophy

Cytotoxic T-Lymphocyte–Associated Protein 4 Fused to a Modified Fragment of IgG1 Reduces Muscle Fiber Damage in a Model of Duchenne Muscular Dystrophy by Attenuating Proinflammatory Gene Expression in Myeloid Lineage Cells

Aging: a Struggle for Beneficial to Overcome Negative Factors made by Muscle and Bone.

Functional cardiac consequences of β-adrenergic stress-induced injury in the mdx mouse model of Duchenne muscular dystrophy

Regulation of injury-induced skeletal myofiber regeneration by glucose transporter 4 (GLUT4)

Both enantiomers of β-aminoisobutyric acid BAIBA regulate Fgf23 via MRGPRD receptor by activating distinct signaling pathways in osteocytes.

Myeloid cell‐specific mutation of Spi1 selectively reduces M2‐biased macrophage numbers in skeletal muscle, reduces age‐related muscle fibrosis and prevents sarcopenia

Muscle-Specific Ablation of Glucose Transporter 1 (GLUT1) Does Not Impair Basal or Overload-Stimulated Skeletal Muscle Glucose Uptake

Myeloid cell-mediated targeting of LIF to dystrophic muscle causes transient increases in muscle fiber lesions by disrupting the recruitment and dispersion of macrophages in muscle.

Differential Effects of Myeloid Cell PPARδ and IL-10 in Regulating Macrophage Recruitment, Phenotype, and Regeneration following Acute Muscle Injury

Collaborators (5)

James G. Tidball

Geoffrey D. Holman

Paul W Hruz

Craig Goergen

E. Dale Abel

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