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The scientific basis for novel treatments of systemic sclerosis.

F1000 medicine reports

Beyer C, Distler JH.
PMID: 20948682
F1000 Med Rep. 2009 Dec 09;1. doi: 10.3410/M1-95.

In recent years, many potential antifibrotic treatment strategies have emerged from molecular studies of systemic sclerosis. Few biologicals have already entered clinical trials and these may hopefully prove to be effective in this progressive, profibrotic disease.

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Beyer C, Distler JH. The scientific basis for novel treatments of systemic sclerosis. F1000 Med Rep. 2009;1doi: 10.3410/M1-95.
Beyer, C., & Distler, J. H. (2009). The scientific basis for novel treatments of systemic sclerosis. F1000 medicine reports, 1. https://doi.org/10.3410/M1-95
Beyer, Christian, and Distler, Jörg Hw. "The scientific basis for novel treatments of systemic sclerosis." F1000 medicine reports vol. 1 (2009). doi: https://doi.org/10.3410/M1-95
Beyer C, Distler JH. The scientific basis for novel treatments of systemic sclerosis. F1000 Med Rep. 2009 Dec 09;1. doi: 10.3410/M1-95. PMID: 20948682; PMCID: PMC2948335.
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Author Correction: Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosis.

Nature communications

Chakraborty D, Šumová B, Mallano T, Chen CW, Distler A, Bergmann C, Ludolph I, Horch RE, Gelse K, Ramming A, Distler O, Schett G, Šenolt L, Distler JHW.
PMID: 34880239
Nat Commun. 2021 Dec 08;12(1):7259. doi: 10.1038/s41467-021-27450-x.

No abstract available.

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Chakraborty D, Šumová B, Mallano T, et al. Author Correction: Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosis. Nat Commun. 2021;12(1):7259doi: 10.1038/s41467-021-27450-x.
Chakraborty, D., Šumová, B., Mallano, T., Chen, C. W., Distler, A., Bergmann, C., Ludolph, I., Horch, R. E., Gelse, K., Ramming, A., Distler, O., Schett, G., Šenolt, L., & Distler, J. H. W. (2021). Author Correction: Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosis. Nature communications, 12(1), 7259. https://doi.org/10.1038/s41467-021-27450-x
Chakraborty, Debomita, et al. "Author Correction: Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosis." Nature communications vol. 12,1 (2021): 7259. doi: https://doi.org/10.1038/s41467-021-27450-x
Chakraborty D, Šumová B, Mallano T, Chen CW, Distler A, Bergmann C, Ludolph I, Horch RE, Gelse K, Ramming A, Distler O, Schett G, Šenolt L, Distler JHW. Author Correction: Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosis. Nat Commun. 2021 Dec 08;12(1):7259. doi: 10.1038/s41467-021-27450-x. PMID: 34880239; PMCID: PMC8655015.
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Platelet Phagocytosis via P-selectin Glycoprotein Ligand 1 and Accumulation of Microparticles in Systemic Sclerosis.

Arthritis & rheumatology (Hoboken, N.J.)

Manfredi AA, Ramirez GA, Godino C, Capobianco A, Monno A, Franchini S, Tombetti E, Corradetti S, Distler JHW, Bianchi ME, Rovere-Querini P, Maugeri N.
PMID: 34279048
Arthritis Rheumatol. 2021 Jul 19; doi: 10.1002/art.41926. Epub 2021 Jul 19.

OBJECTIVE: It is unclear why activated platelets and platelet-derived microparticles (MPs) accumulate in the blood of patients with systemic sclerosis (SSc). This study was undertaken to investigate whether defective phagocytosis might contribute to MP accumulation in the blood of...

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Manfredi AA, Ramirez GA, Godino C, et al. Platelet Phagocytosis via P-selectin Glycoprotein Ligand 1 and Accumulation of Microparticles in Systemic Sclerosis. Arthritis Rheumatol. 2021;doi: 10.1002/art.41926.
Manfredi, A. A., Ramirez, G. A., Godino, C., Capobianco, A., Monno, A., Franchini, S., Tombetti, E., Corradetti, S., Distler, J. H. W., Bianchi, M. E., Rovere-Querini, P., & Maugeri, N. (2021). Platelet Phagocytosis via P-selectin Glycoprotein Ligand 1 and Accumulation of Microparticles in Systemic Sclerosis. Arthritis & rheumatology (Hoboken, N.J.), . https://doi.org/10.1002/art.41926
Manfredi, Angelo A, et al. "Platelet Phagocytosis via P-selectin Glycoprotein Ligand 1 and Accumulation of Microparticles in Systemic Sclerosis." Arthritis & rheumatology (Hoboken, N.J.) vol. (2021). doi: https://doi.org/10.1002/art.41926
Manfredi AA, Ramirez GA, Godino C, Capobianco A, Monno A, Franchini S, Tombetti E, Corradetti S, Distler JHW, Bianchi ME, Rovere-Querini P, Maugeri N. Platelet Phagocytosis via P-selectin Glycoprotein Ligand 1 and Accumulation of Microparticles in Systemic Sclerosis. Arthritis Rheumatol. 2021 Jul 19; doi: 10.1002/art.41926. Epub 2021 Jul 19. PMID: 34279048.
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Bone Morphogenetic Protein Antagonist Gremlin-1 Increases Myofibroblast Transition in Dermal Fibroblasts: Implications for Systemic Sclerosis.

Frontiers in cell and developmental biology

Duffy L, Henderson J, Brown M, Pryzborski S, Fullard N, Summa L, Distler JHW, Stratton R, O'Reilly S.
PMID: 34150776
Front Cell Dev Biol. 2021 Jun 04;9:681061. doi: 10.3389/fcell.2021.681061. eCollection 2021.

OBJECTIVE: Systemic Sclerosis is an autoimmune connective tissue disease which results in fibrosis of the skin and lungs. The disease is characterized by activation of myofibroblasts but what governs this is unknown. Gremlin-1 is a BMP antagonist that is...

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Duffy L, Henderson J, Brown M, et al. Bone Morphogenetic Protein Antagonist Gremlin-1 Increases Myofibroblast Transition in Dermal Fibroblasts: Implications for Systemic Sclerosis. Front Cell Dev Biol. 2021;9:681061doi: 10.3389/fcell.2021.681061.
Duffy, L., Henderson, J., Brown, M., Pryzborski, S., Fullard, N., Summa, L., Distler, J. H. W., Stratton, R., & O'Reilly, S. (2021). Bone Morphogenetic Protein Antagonist Gremlin-1 Increases Myofibroblast Transition in Dermal Fibroblasts: Implications for Systemic Sclerosis. Frontiers in cell and developmental biology, 9681061. https://doi.org/10.3389/fcell.2021.681061
Duffy, Laura, et al. "Bone Morphogenetic Protein Antagonist Gremlin-1 Increases Myofibroblast Transition in Dermal Fibroblasts: Implications for Systemic Sclerosis." Frontiers in cell and developmental biology vol. 9 (2021): 681061. doi: https://doi.org/10.3389/fcell.2021.681061
Duffy L, Henderson J, Brown M, Pryzborski S, Fullard N, Summa L, Distler JHW, Stratton R, O'Reilly S. Bone Morphogenetic Protein Antagonist Gremlin-1 Increases Myofibroblast Transition in Dermal Fibroblasts: Implications for Systemic Sclerosis. Front Cell Dev Biol. 2021 Jun 04;9:681061. doi: 10.3389/fcell.2021.681061. eCollection 2021. PMID: 34150776; PMCID: PMC8213337.
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Impaired TFAM expression promotes mitochondrial damage to drive fibroblast activation and fibrosis in systemic sclerosis.

Arthritis & rheumatology (Hoboken, N.J.)

Zhou X, Trinh-Minh T, Tran-Manh C, Gießl A, Bergmann C, Györfi AH, Schett G, Distler JHW.
PMID: 34807516
Arthritis Rheumatol. 2021 Nov 22; doi: 10.1002/art.42033. Epub 2021 Nov 22.

OBJECTIVES: The transcription factor TFAM is controlling the transcription of core proteins required for mitochondrial homeostasis. The aim of the current study was to investigate changes in TFAM expression in systemic sclerosis (SSc), to analyze mitochondrial function and to...

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Zhou X, Trinh-Minh T, Tran-Manh C, et al. Impaired TFAM expression promotes mitochondrial damage to drive fibroblast activation and fibrosis in systemic sclerosis. Arthritis Rheumatol. 2021;doi: 10.1002/art.42033.
Zhou, X., Trinh-Minh, T., Tran-Manh, C., Gießl, A., Bergmann, C., Györfi, A. H., Schett, G., & Distler, J. H. W. (2021). Impaired TFAM expression promotes mitochondrial damage to drive fibroblast activation and fibrosis in systemic sclerosis. Arthritis & rheumatology (Hoboken, N.J.), . https://doi.org/10.1002/art.42033
Zhou, Xiang, et al. "Impaired TFAM expression promotes mitochondrial damage to drive fibroblast activation and fibrosis in systemic sclerosis." Arthritis & rheumatology (Hoboken, N.J.) vol. (2021). doi: https://doi.org/10.1002/art.42033
Zhou X, Trinh-Minh T, Tran-Manh C, Gießl A, Bergmann C, Györfi AH, Schett G, Distler JHW. Impaired TFAM expression promotes mitochondrial damage to drive fibroblast activation and fibrosis in systemic sclerosis. Arthritis Rheumatol. 2021 Nov 22; doi: 10.1002/art.42033. Epub 2021 Nov 22. PMID: 34807516.
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Author Correction: Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosis.

Nature communications

Chakraborty D, Šumová B, Mallano T, Chen CW, Distler A, Bergmann C, Ludolph I, Horch RE, Gelse K, Ramming A, Distler O, Schett G, Šenolt L, Distler JHW.
PMID: 34880239
Nat Commun. 2021 Dec 08;12(1):7259. doi: 10.1038/s41467-021-27450-x.

No abstract available.

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Chakraborty D, Šumová B, Mallano T, et al. Author Correction: Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosis. Nat Commun. 2021;12(1):7259doi: 10.1038/s41467-021-27450-x.
Chakraborty, D., Šumová, B., Mallano, T., Chen, C. W., Distler, A., Bergmann, C., Ludolph, I., Horch, R. E., Gelse, K., Ramming, A., Distler, O., Schett, G., Šenolt, L., & Distler, J. H. W. (2021). Author Correction: Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosis. Nature communications, 12(1), 7259. https://doi.org/10.1038/s41467-021-27450-x
Chakraborty, Debomita, et al. "Author Correction: Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosis." Nature communications vol. 12,1 (2021): 7259. doi: https://doi.org/10.1038/s41467-021-27450-x
Chakraborty D, Šumová B, Mallano T, Chen CW, Distler A, Bergmann C, Ludolph I, Horch RE, Gelse K, Ramming A, Distler O, Schett G, Šenolt L, Distler JHW. Author Correction: Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosis. Nat Commun. 2021 Dec 08;12(1):7259. doi: 10.1038/s41467-021-27450-x. PMID: 34880239.
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Targeting of canonical WNT signaling ameliorates experimental sclerodermatous chronic graft-versus-host disease.

Blood

Zhang Y, Shen L, Dreißigacker K, Zhu H, Trinh-Minh T, Meng X, Tran-Manh C, Dees C, Matei AE, Chen CW, Ditschkowski M, Krauss S, Winkler J, Wolff D, Ziemer M, Beilhack A, Karrer S, Herr W, Mackensen A, Schett G, Spriewald BM, Distler JHW.
PMID: 33529322
Blood. 2021 Apr 29;137(17):2403-2416. doi: 10.1182/blood.2020008720.

Chronic graft-versus-host disease (cGVHD) is a major life-threatening complication of allogeneic hematopoietic stem cell transplantation. The molecular mechanisms underlying cGVHD remain poorly understood, and targeted therapies for clinical use are not well established. Here, we examined the role of...

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Zhang Y, Shen L, Dreißigacker K, et al. Targeting of canonical WNT signaling ameliorates experimental sclerodermatous chronic graft-versus-host disease. Blood. 2021;137(17):2403-2416doi: 10.1182/blood.2020008720.
Zhang, Y., Shen, L., Dreißigacker, K., Zhu, H., Trinh-Minh, T., Meng, X., Tran-Manh, C., Dees, C., Matei, A. E., Chen, C. W., Ditschkowski, M., Krauss, S., Winkler, J., Wolff, D., Ziemer, M., Beilhack, A., Karrer, S., Herr, W., Mackensen, A., Schett, G., Spriewald, B. M., & Distler, J. H. W. (2021). Targeting of canonical WNT signaling ameliorates experimental sclerodermatous chronic graft-versus-host disease. Blood, 137(17), 2403-2416. https://doi.org/10.1182/blood.2020008720
Zhang, Yun, et al. "Targeting of canonical WNT signaling ameliorates experimental sclerodermatous chronic graft-versus-host disease." Blood vol. 137,17 (2021): 2403-2416. doi: https://doi.org/10.1182/blood.2020008720
Zhang Y, Shen L, Dreißigacker K, Zhu H, Trinh-Minh T, Meng X, Tran-Manh C, Dees C, Matei AE, Chen CW, Ditschkowski M, Krauss S, Winkler J, Wolff D, Ziemer M, Beilhack A, Karrer S, Herr W, Mackensen A, Schett G, Spriewald BM, Distler JHW. Targeting of canonical WNT signaling ameliorates experimental sclerodermatous chronic graft-versus-host disease. Blood. 2021 Apr 29;137(17):2403-2416. doi: 10.1182/blood.2020008720. PMID: 33529322.
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Estimated glomerular filtration rate is a marker of mortality in the European Scleroderma Trials and Research Group (EUSTAR) database.

Rheumatology (Oxford, England)

Gigante A, Hoffmann-Vold AM, Alunni Fegatelli D, Gabrielli A, Leodori G, Coleiro B, De Santis M, Dagna L, Alegre-Sancho JJ, Montecucco C, Carreira PE, Balbir-Gurman A, Doria A, Riemekasten G, Airò P, Distler J, Distler O, Rosato E.
PMID: 33769468
Rheumatology (Oxford). 2021 Dec 24;61(1):213-222. doi: 10.1093/rheumatology/keab302.

OBJECTIVES: The study aim was to evaluate the estimated glomerular filtration rate (eGFR), its association with clinical disease and its predictive ability with respect to mortality in SSc patients from the European Scleroderma Trials and Research Group (EUSTAR) database.METHODS:...

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Gigante A, Hoffmann-Vold AM, Alunni Fegatelli D, et al. Estimated glomerular filtration rate is a marker of mortality in the European Scleroderma Trials and Research Group (EUSTAR) database. Rheumatology (Oxford). 2021;61(1):213-222doi: 10.1093/rheumatology/keab302.
Gigante, A., Hoffmann-Vold, A. M., Alunni Fegatelli, D., Gabrielli, A., Leodori, G., Coleiro, B., De Santis, M., Dagna, L., Alegre-Sancho, J. J., Montecucco, C., Carreira, P. E., Balbir-Gurman, A., Doria, A., Riemekasten, G., Airò, P., Distler, J., Distler, O., Rosato, E. (2021). Estimated glomerular filtration rate is a marker of mortality in the European Scleroderma Trials and Research Group (EUSTAR) database. Rheumatology (Oxford, England), 61(1), 213-222. https://doi.org/10.1093/rheumatology/keab302
Gigante, Antonietta, et al. "Estimated glomerular filtration rate is a marker of mortality in the European Scleroderma Trials and Research Group (EUSTAR) database." Rheumatology (Oxford, England) vol. 61,1 (2021): 213-222. doi: https://doi.org/10.1093/rheumatology/keab302
Gigante A, Hoffmann-Vold AM, Alunni Fegatelli D, Gabrielli A, Leodori G, Coleiro B, De Santis M, Dagna L, Alegre-Sancho JJ, Montecucco C, Carreira PE, Balbir-Gurman A, Doria A, Riemekasten G, Airò P, Distler J, Distler O, Rosato E. Estimated glomerular filtration rate is a marker of mortality in the European Scleroderma Trials and Research Group (EUSTAR) database. Rheumatology (Oxford). 2021 Dec 24;61(1):213-222. doi: 10.1093/rheumatology/keab302. PMID: 33769468.
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Chemokines and chemokine receptors in the pathogenesis of systemic sclerosis.

Modern rheumatology

Distler O, Distler J, Kowal-Bielecka O, Gay RE, Müller-Ladner U, Gay S.
PMID: 24383897
Mod Rheumatol. 2002 Jun;12(2):107-12. doi: 10.3109/s101650200019.

Abstract  Activation of the immune system and increased synthesis of extracellular matrix proteins by fibroblasts are hallmarks in the pathogenesis of systemic sclerosis (SSc). The mechanisms that initiate the accumulation of inflammatory cells are still unknown. Chemokines are a...

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Distler O, Distler J, Kowal-Bielecka O, et al. Chemokines and chemokine receptors in the pathogenesis of systemic sclerosis. Mod Rheumatol. 2002;12(2):107-12doi: 10.3109/s101650200019.
Distler, O., Distler, J., Kowal-Bielecka, O., Gay, R. E., Müller-Ladner, U., & Gay, S. (2002). Chemokines and chemokine receptors in the pathogenesis of systemic sclerosis. Modern rheumatology, 12(2), 107-12. https://doi.org/10.3109/s101650200019
Distler, O, et al. "Chemokines and chemokine receptors in the pathogenesis of systemic sclerosis." Modern rheumatology vol. 12,2 (2002): 107-12. doi: https://doi.org/10.3109/s101650200019
Distler O, Distler J, Kowal-Bielecka O, Gay RE, Müller-Ladner U, Gay S. Chemokines and chemokine receptors in the pathogenesis of systemic sclerosis. Mod Rheumatol. 2002 Jun;12(2):107-12. doi: 10.3109/s101650200019. PMID: 24383897.
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Falsifying models of new physics via WW scattering.

Physical review letters

Distler J, Grinstein B, Porto RA, Rothstein IZ.
PMID: 17358753
Phys Rev Lett. 2007 Jan 26;98(4):041601. doi: 10.1103/PhysRevLett.98.041601. Epub 2007 Jan 22.

We show that the coefficients of operators in the electroweak chiral Lagrangian can be bounded if the underlying theory obeys the usual assumptions of Lorentz invariance, analyticity, unitarity, and crossing to arbitrarily short distances. Violations of these bounds can...

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Distler J, Grinstein B, Porto RA, et al. Falsifying models of new physics via WW scattering. Phys Rev Lett. 2007;98(4):041601doi: 10.1103/PhysRevLett.98.041601.
Distler, J., Grinstein, B., Porto, R. A., & Rothstein, I. Z. (2007). Falsifying models of new physics via WW scattering. Physical review letters, 98(4), 041601. https://doi.org/10.1103/PhysRevLett.98.041601
Distler, Jacques, et al. "Falsifying models of new physics via WW scattering." Physical review letters vol. 98,4 (2007): 041601. doi: https://doi.org/10.1103/PhysRevLett.98.041601
Distler J, Grinstein B, Porto RA, Rothstein IZ. Falsifying models of new physics via WW scattering. Phys Rev Lett. 2007 Jan 26;98(4):041601. doi: 10.1103/PhysRevLett.98.041601. Epub 2007 Jan 22. PMID: 17358753.
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Metabolic Aspects of Neurospora Activation and Germination.

Plant physiology

Sussman AS, Distler JR, Krakow JS.
PMID: 16654847
Plant Physiol. 1956 Mar;31(2):126-35. doi: 10.1104/pp.31.2.126.

No abstract available.

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Sussman AS, Distler JR, Krakow JS. Metabolic Aspects of Neurospora Activation and Germination. Plant Physiol. 1956;31(2):126-35doi: 10.1104/pp.31.2.126.
Sussman, A. S., Distler, J. R., & Krakow, J. S. (1956). Metabolic Aspects of Neurospora Activation and Germination. Plant physiology, 31(2), 126-35. https://doi.org/10.1104/pp.31.2.126
Sussman, A S, et al. "Metabolic Aspects of Neurospora Activation and Germination." Plant physiology vol. 31,2 (1956): 126-35. doi: https://doi.org/10.1104/pp.31.2.126
Sussman AS, Distler JR, Krakow JS. Metabolic Aspects of Neurospora Activation and Germination. Plant Physiol. 1956 Mar;31(2):126-35. doi: 10.1104/pp.31.2.126. PMID: 16654847; PMCID: PMC540744.
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Small Molecule Tyrosine Kinase Inhibitor Nintedanib Reduces Development of Cardiac Allograft Vasculopathy in Murine Aortic Allografts.

Transplantation direct

Gocht A, Spriewald B, Distler JHW, Ramsperger-Gleixner M, Ensminger SM, Weyand M, Heim C, Jude EB, Eleftheriadou I, Tentolouris N.
PMID: 30046657
Transplant Direct. 2018 Jun 18;4(7):e367. doi: 10.1097/TXD.0000000000000804. eCollection 2018 Jul.

BACKGROUND: Nintedanib is a small molecule tyrosine kinase inhibitor that blocks the action of the platelet-derived growth factor receptor (PDGFR), the vascular endothelial growth factor receptor (VEGFR) and the fibroblast growth factor receptor. All of these receptors have been...

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Gocht A, Spriewald B, Distler JHW, et al. Small Molecule Tyrosine Kinase Inhibitor Nintedanib Reduces Development of Cardiac Allograft Vasculopathy in Murine Aortic Allografts. Transplant Direct. 2018;4(7):e367doi: 10.1097/TXD.0000000000000804.
Gocht, A., Spriewald, B., Distler, J. H. W., Ramsperger-Gleixner, M., Ensminger, S. M., Weyand, M., Heim, C., Jude, E. B., Eleftheriadou, I., & Tentolouris, N. (2018). Small Molecule Tyrosine Kinase Inhibitor Nintedanib Reduces Development of Cardiac Allograft Vasculopathy in Murine Aortic Allografts. Transplantation direct, 4(7), e367. https://doi.org/10.1097/TXD.0000000000000804
Gocht, Annika, et al. "Small Molecule Tyrosine Kinase Inhibitor Nintedanib Reduces Development of Cardiac Allograft Vasculopathy in Murine Aortic Allografts." Transplantation direct vol. 4,7 (2018): e367. doi: https://doi.org/10.1097/TXD.0000000000000804
Gocht A, Spriewald B, Distler JHW, Ramsperger-Gleixner M, Ensminger SM, Weyand M, Heim C, Jude EB, Eleftheriadou I, Tentolouris N. Small Molecule Tyrosine Kinase Inhibitor Nintedanib Reduces Development of Cardiac Allograft Vasculopathy in Murine Aortic Allografts. Transplant Direct. 2018 Jun 18;4(7):e367. doi: 10.1097/TXD.0000000000000804. eCollection 2018 Jul. PMID: 30046657; PMCID: PMC6056280.
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Showing 25 to 36 of 38 entries