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  1. Article ; Online: Remembering Eberhard Ritz: A Clinician-Scientist Extraordinaire.

    Reiser, Jochen / Zeier, Martin

    Journal of the American Society of Nephrology : JASN

    2024  Volume 35, Issue 4, Page(s) 515–516

    MeSH term(s) Humans ; Physicians ; Biomedical Research
    Language English
    Publishing date 2024-01-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.0000000000000304
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    Zs.A 3344: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  2. Article ; Online: XOR risk variants drive diabetic kidney disease.

    Zhu, Ke / Reiser, Jochen

    Nature metabolism

    2023  Volume 5, Issue 4, Page(s) 536–537

    MeSH term(s) Humans ; Diabetic Nephropathies/genetics ; Diabetes Mellitus
    Language English
    Publishing date 2023-04-06
    Publishing country Germany
    Document type Journal Article ; Comment
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-023-00768-0
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  3. Book ; Thesis: Pathobiologie der Podozyten

    Reiser, Jochen

    molekulare Analyse der glomerulären Schlitzmembran und Fortsatzdynamik von Podozyten

    1998  

    Author's details vorgelegt von Jochen Reiser
    Language German
    Size 77 Bl. : Ill., graph. Darst.
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Heidelberg, Univ., Diss., 1999 (Nicht für den Austausch)
    HBZ-ID HT011210232
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2000 E 404 order for loan Magazin

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  4. Article ; Online: ALKBH1 reduces DNA N6-methyladenine to allow for vascular calcification in chronic kidney disease.

    Zhu, Ke / Reiser, Jochen

    The Journal of clinical investigation

    2021  Volume 131, Issue 14

    Abstract: Vascular calcification is a common complication of chronic kidney disease (CKD), and one of the main risk factors for increased cardiovascular morbidity and mortality in patients with CKD. In this issue of the JCI, Ouyang and Su et al. report that Alkb ... ...

    Abstract Vascular calcification is a common complication of chronic kidney disease (CKD), and one of the main risk factors for increased cardiovascular morbidity and mortality in patients with CKD. In this issue of the JCI, Ouyang and Su et al. report that Alkb homolog 1 (ALKBH1), a DNA demethylase, reduced DNA N6-methyladenine (6mA) in vascular smooth muscle cells (VSMCs) and leukocytes, thus leading to aortic arch calcification in the patients with CKD. During the progression of vascular calcification, increased ALKBH1 expression was linked to decreased 6mA levels, findings that the authors noted in both patients with CKD and CKD mouse models. The kidney and vascular disease risk factor soluble urokinase receptor (suPAR) was also elevated in the plasma. Notably, lower 6mA levels induced BMP2-mediated osteogenic reprogramming in the VSMCs. These findings present a function of ALKBH1 in vascular calcification and provide a framework for therapeutic strategies.
    MeSH term(s) AlkB Homolog 1, Histone H2a Dioxygenase ; Animals ; DNA ; Humans ; Mice ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle ; Renal Insufficiency, Chronic/genetics ; Vascular Calcification/genetics
    Chemical Substances DNA (9007-49-2) ; ALKBH1 protein, human (EC 1.14.11.33) ; AlkB Homolog 1, Histone H2a Dioxygenase (EC 1.14.11.33)
    Language English
    Publishing date 2021-07-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI150966
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  5. Article ; Online: SARS-CoV-2 pirates the kidneys: A scar(y) story.

    Reiser, Jochen / Spear, Ryan / Luo, Shengyuan

    Cell metabolism

    2022  Volume 34, Issue 3, Page(s) 352–354

    Abstract: SARS-CoV-2 can cause diverse severe and lasting damage to the kidneys. In the latest issue of Cell Stem Cell, Jansen et al. utilized data gleaned from human kidney autopsies and human induced pluripotent stem cell-derived kidney organoids to investigate ... ...

    Abstract SARS-CoV-2 can cause diverse severe and lasting damage to the kidneys. In the latest issue of Cell Stem Cell, Jansen et al. utilized data gleaned from human kidney autopsies and human induced pluripotent stem cell-derived kidney organoids to investigate the direct effects of SARS-CoV-2 infection on kidney cells. They found that such infections resulted in renal scarring (notably, tubulointerstitial fibrosis).
    MeSH term(s) COVID-19 ; Cicatrix ; Humans ; Induced Pluripotent Stem Cells ; Kidney ; SARS-CoV-2
    Language English
    Publishing date 2022-03-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2022.02.005
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  6. Article: suPAR: An Inflammatory Mediator for Kidneys.

    Sudhini, Yashwanth Reddy / Wei, Changli / Reiser, Jochen

    Kidney diseases (Basel, Switzerland)

    2022  Volume 8, Issue 4, Page(s) 265–274

    Abstract: Background: Inflammation is a common feature of many kidney diseases. The implicated inflammatory mediators and their underlying molecular mechanisms however are often not clear.: Summary: suPAR is the soluble form of urokinase-type plasminogen ... ...

    Abstract Background: Inflammation is a common feature of many kidney diseases. The implicated inflammatory mediators and their underlying molecular mechanisms however are often not clear.
    Summary: suPAR is the soluble form of urokinase-type plasminogen activator receptor (uPAR), associated with inflammation and immune activation. It has evolved into a unique circulating kidney disease factor over the last 10 years. In particular, suPAR has multiple looks due to enzymatic cleavage and alternative transcriptional splicing of the uPAR gene. Most recently, suPAR has emerged as a systemic mediator for COVID-19 infection, associated with lung as well as kidney dysfunction. Like membrane-bound uPAR, suPAR could interact with integrins (e.g., αvβ3 integrin) on podocytes, providing the molecular basis for some glomerular kidney diseases. In addition, there have been numerous studies suggesting that suPAR connects acute kidney injury to chronic kidney disease as a special kidney risk factor. Moreover, the implication of circulating suPAR levels in kidney transplantation and plasmapheresis not only indicates its relevance in monitoring for recurrence but also implies suPAR as a possible therapeutic target. In fact, the therapeutic concept of manipulating suPAR function has been evidenced in several kidney disease experimental models.
    Key messages: The last 10 years of research has established suPAR as a unique inflammatory mediator for kidneys. While open questions remain and deserve additional studies, modulating suPAR function may represent a promising novel therapeutic strategy for kidney disease.
    Language English
    Publishing date 2022-06-08
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2817963-8
    ISSN 2296-9357 ; 2296-9381
    ISSN (online) 2296-9357
    ISSN 2296-9381
    DOI 10.1159/000524965
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  7. Article: suPAR, a Circulating Kidney Disease Factor.

    Wei, Changli / Spear, Ryan / Hahm, Eunsil / Reiser, Jochen

    Frontiers in medicine

    2021  Volume 8, Page(s) 745838

    Abstract: Urokinase plasminogen activator receptor (uPAR) is a multifaceted, GPI-anchored three-domain protein. Release of the receptor results in variable levels of soluble uPAR (suPAR) in the blood circulation. suPAR levels have been linked to many disease ... ...

    Abstract Urokinase plasminogen activator receptor (uPAR) is a multifaceted, GPI-anchored three-domain protein. Release of the receptor results in variable levels of soluble uPAR (suPAR) in the blood circulation. suPAR levels have been linked to many disease states. In this mini-review, we discuss suPAR as a key circulating molecule mediating kidney disease with a particular focus on differently spliced isoforms.
    Language English
    Publishing date 2021-10-06
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2775999-4
    ISSN 2296-858X
    ISSN 2296-858X
    DOI 10.3389/fmed.2021.745838
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  8. Article ; Online: suPAR

    Yashwanth Reddy Sudhini / Changli Wei / Jochen Reiser

    Kidney Diseases, Vol 8, Iss 4, Pp 265-

    An Inflammatory Mediator for Kidneys

    2022  Volume 274

    Abstract: Background: Inflammation is a common feature of many kidney diseases. The implicated inflammatory mediators and their underlying molecular mechanisms however are often not clear. Summary: suPAR is the soluble form of urokinase-type plasminogen activator ... ...

    Abstract Background: Inflammation is a common feature of many kidney diseases. The implicated inflammatory mediators and their underlying molecular mechanisms however are often not clear. Summary: suPAR is the soluble form of urokinase-type plasminogen activator receptor (uPAR), associated with inflammation and immune activation. It has evolved into a unique circulating kidney disease factor over the last 10 years. In particular, suPAR has multiple looks due to enzymatic cleavage and alternative transcriptional splicing of the uPAR gene. Most recently, suPAR has emerged as a systemic mediator for COVID-19 infection, associated with lung as well as kidney dysfunction. Like membrane-bound uPAR, suPAR could interact with integrins (e.g., αvβ3 integrin) on podocytes, providing the molecular basis for some glomerular kidney diseases. In addition, there have been numerous studies suggesting that suPAR connects acute kidney injury to chronic kidney disease as a special kidney risk factor. Moreover, the implication of circulating suPAR levels in kidney transplantation and plasmapheresis not only indicates its relevance in monitoring for recurrence but also implies suPAR as a possible therapeutic target. In fact, the therapeutic concept of manipulating suPAR function has been evidenced in several kidney disease experimental models. Key Messages: The last 10 years of research has established suPAR as a unique inflammatory mediator for kidneys. While open questions remain and deserve additional studies, modulating suPAR function may represent a promising novel therapeutic strategy for kidney disease.
    Keywords soluble urokinase-type plasminogen activator receptor ; kidney ; integrin ; covid-19 ; biomarker ; therapeutics ; Internal medicine ; RC31-1245
    Subject code 616
    Language English
    Publishing date 2022-06-01T00:00:00Z
    Publisher Karger Publishers
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Reduced Bioactive Microbial Products (Pathogen-Associated Molecular Patterns) Contribute to Dysregulated Immune Responses and Impaired Healing in Infected Wounds in Mice with Diabetes.

    Roy, Ruchi / Mahmud, Foyez / Zayas, Janet / Kuzel, Timothy M / Reiser, Jochen / Shafikhani, Sasha H

    The Journal of investigative dermatology

    2023  Volume 144, Issue 2, Page(s) 387–397.e11

    Abstract: Diabetic chronic ulcers are plagued with persistent nonresolving inflammation. However, diabetic wound environment early after injury suffers from inadequate inflammatory responses due to reductions in proinflammatory cytokines levels. Diabetic ... ...

    Abstract Diabetic chronic ulcers are plagued with persistent nonresolving inflammation. However, diabetic wound environment early after injury suffers from inadequate inflammatory responses due to reductions in proinflammatory cytokines levels. Diabetic neutrophils have known impairments in bactericidal functions. We hypothesized that reduced bacterial killing by diabetic neutrophils, due to their bactericidal functional impairments, results in reduced bioactive bacterial products, known as pathogen-associated molecular patterns, which in turn contribute to reduced signaling through toll-like receptors, leading to inadequate production of proinflammatory cytokines in infected diabetic wound early after injury. We tested our hypothesis in db/db type 2 obese diabetic mouse wound infection model with Pseudomonas aeruginosa. Our data indicate that despite substantially higher levels of infection, toll-like receptor 4-mediated signaling is reduced in diabetic wounds early after injury owing to reduced bioactive levels of lipopolysaccharide. We further demonstrate that topical treatment with lipopolysaccharide enhances toll-like receptor 4 signaling, increases proinflammatory cytokine production, restores leukocyte trafficking, reduces infection burden, and stimulates healing in diabetic wounds. We posit that lipopolysaccharide may be a viable therapeutic option for the treatment of diabetic foot ulcers if it is applied topically after the surgical debridement process, which is intended to reset chronic ulcers into acute fresh wounds.
    MeSH term(s) Mice ; Animals ; Toll-Like Receptor 4 ; Pathogen-Associated Molecular Pattern Molecules/therapeutic use ; Lipopolysaccharides ; Wound Infection/drug therapy ; Diabetic Foot/drug therapy ; Diabetes Mellitus, Type 2 ; Anti-Bacterial Agents/therapeutic use ; Immunity ; Cytokines
    Chemical Substances Toll-Like Receptor 4 ; Pathogen-Associated Molecular Pattern Molecules ; Lipopolysaccharides ; Anti-Bacterial Agents ; Cytokines
    Language English
    Publishing date 2023-08-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80136-7
    ISSN 1523-1747 ; 0022-202X
    ISSN (online) 1523-1747
    ISSN 0022-202X
    DOI 10.1016/j.jid.2023.08.004
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  10. Article ; Online: More expression, less function: cleaved dynamin in glomerular kidney disease.

    Altintas, Mehmet M / Reiser, Jochen

    The Journal of pathology

    2019  Volume 247, Issue 4, Page(s) 413–415

    Abstract: The role of dynamin in regulation of kidney filtration barrier is well documented. Dynamin binds to and produces filamentous actin, which is a key component of healthy podocyte foot processes (FPs). Destruction of dynamin, for example by cathepsin L, ... ...

    Abstract The role of dynamin in regulation of kidney filtration barrier is well documented. Dynamin binds to and produces filamentous actin, which is a key component of healthy podocyte foot processes (FPs). Destruction of dynamin, for example by cathepsin L, leads to loss of a functional actin network and uncoordinated membrane signaling, a situation that allows for effacement of FPs and proteinuria. Now, Khalil et al have examined the dynamin expression in kidneys of proteinuric animal models as well as in kidney patients and produced data that further clarifies the role of dynamin in glomerular and tubular proteinuria and may aid in pinpointing patients who are affected by loss of dynamin function and may benefit from appropriate therapeutic approaches. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    MeSH term(s) Animals ; Dynamins ; Humans ; Kidney Diseases ; Podocytes ; Proteinuria ; United Kingdom
    Chemical Substances Dynamins (EC 3.6.5.5)
    Language English
    Publishing date 2019-01-25
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 3119-7
    ISSN 1096-9896 ; 0022-3417
    ISSN (online) 1096-9896
    ISSN 0022-3417
    DOI 10.1002/path.5217
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