M
Martin Lotz
Researcher at Scripps Research Institute
Publications - 382
Citations - 33862
Martin Lotz is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Cartilage & Chondrocyte. The author has an hindex of 97, co-authored 343 publications receiving 30942 citations. Previous affiliations of Martin Lotz include Japan Agency for Medical Research and Development & University of California, San Diego.
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Journal ArticleDOI
Cytokines in cartilage injury and repair.
TL;DR: Insight into intracellular signaling mechanisms that are activated by cytokines may provide the basis for pharmacologic interventions that promote cartilage repair.
Journal ArticleDOI
Inflammation-induced chondrocyte hypertrophy is driven by receptor for advanced glycation end products.
Denise L. Cecil,Kristen Johnson,John Rediske,Martin Lotz,Ann Marie Schmidt,Robert Terkeltaub +5 more
TL;DR: It is concluded that up-regulated chondrocyte expression of the RAGE ligand S100A11 in OA cartilage, and RAGE signaling through the p38 MAPK pathway, promote inflammation-associated chondROcyte hypertrophy and has the potential to contribute to the progression of OA.
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Integrin expression by human articular chondrocytes.
Virgil L. Woods,Paul J. Schreck,Dirk S. Gesink,Hector O. Pacheco,David Amiel,Wayne H. Akeson,Martin Lotz +6 more
TL;DR: Normal human articular chondrocytes prominently display substantial quantities of the alpha 1 beta 1, alpha 5beta 1, and alpha v beta 5 integrin heterodimers, as well as lesser quantities ofThe alpha 3 beta 1 andalpha v beta 3 heterodIMers.
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FoxO transcription factors support oxidative stress resistance in human chondrocytes.
Yukio Akasaki,Oscar Alvarez-Garcia,Masahiko Saito,Beatriz Caramés,Yukihide Iwamoto,Martin Lotz +5 more
TL;DR: The objective of this study was to investigate the impact of down‐regulated FoxO transcription factors on chondrocytes and found that it is dysregulated in aged and OA cartilage.
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Caspase inhibitors reduce severity of cartilage lesions in experimental osteoarthritis.
TL;DR: Results provide direct support for a role of cell death in OA pathogenesis and reduce the severity of cartilage lesions in experimental OA, suggesting that caspase inhibitors may have disease-modifying activity in human OA.