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Jens Schmidt

Researcher at University of Göttingen

Publications -  77
Citations -  7576

Jens Schmidt is an academic researcher from University of Göttingen. The author has contributed to research in topics: Inclusion body myositis & Skeletal muscle. The author has an hindex of 25, co-authored 73 publications receiving 6706 citations. Previous affiliations of Jens Schmidt include National Institutes of Health & Foundation University, Islamabad.

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IL-1β-Induced Accumulation of Amyloid: Macroautophagy in Skeletal Muscle Depends on ERK

TL;DR: The data demonstrate that the ERK pathway contributes to formation of β-amyloid and regulation of autophagic activity in muscle cells exposed to proinflammatory cell stress and suggests that ERK serves as an important mediator between inflammatory mechanisms and protein deposition in skeletal muscle and is a crucial element of the pathology of IBM.
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Treatment with human immunoglobulin G improves the early disease course in a mouse model of Duchenne muscular dystrophy

TL;DR: It is demonstrated that, in the early disease course of mdx mice, human IgG improves the running performance and diminishes myopathic damage and inflammation in the muscle.
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TNF-α upregulates macroautophagic processing of APP/β-amyloid in a human rhabdomyosarcoma cell line

TL;DR: It is shown that TNF-α-mediated upregulation of macroautophagy modulates APP and β-amyloid load and can be blocked by inhibition of macroAutophagy, which may be a crucial mediator between inflammation andβ-amymyloid-associated degeneration in skeletal muscle.
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Cell stress molecules in the skeletal muscle of GNE myopathy

TL;DR: The cell-stress molecules αB-crystallin and iNOS are overexpressed in GNE myopathy muscle and may identify early disease mechanisms.
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Molecular treatment effects of alemtuzumab in skeletal muscles of patients with IBM.

TL;DR: Alemtuzumab showed a trend towards downregulation of the expression of some inflammatory molecules in skeletal muscle of IBM patients but has no effect on several crucial markers of cell stress and degeneration.