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  1. Article ; Online: Adenine crosses the biomarker bridge: from 'omics to treatment in diabetic kidney disease.

    Drexler, Yelena / Fornoni, Alessia

    The Journal of clinical investigation

    2023  Volume 133, Issue 20

    Abstract: Enabling the early detection and prevention of diabetic kidney damage has potential to substantially reduce the global burden of kidney failure. There is a critical need for identification of mechanistic biomarkers that can predict progression and serve ... ...

    Abstract Enabling the early detection and prevention of diabetic kidney damage has potential to substantially reduce the global burden of kidney failure. There is a critical need for identification of mechanistic biomarkers that can predict progression and serve as therapeutic targets. In this issue of the JCI, Sharma and colleagues used an integrated multiomics approach to identify the metabolite adenine as a noninvasive biomarker of progression in early diabetic kidney disease (DKD). The highest tertile of urine adenine/creatinine ratio (UAdCR) was associated with higher risk for end-stage kidney disease and mortality across independent cohorts, including participants with early DKD without macroalbuminuria. Spatial metabolomics, single-cell transcriptomics, and experimental studies localized adenine to regions of tubular pathology and implicated the mTOR pathway in adenine-mediated tissue fibrosis. Inhibition of endogenous adenine production was protective in a diabetic model. These findings exemplify the potential for multiomics to uncover mechanistic biomarkers and targeted therapies in DKD.
    MeSH term(s) Humans ; Diabetic Nephropathies/diagnosis ; Diabetic Nephropathies/genetics ; Diabetic Nephropathies/metabolism ; Adenine ; Kidney Failure, Chronic/metabolism ; Biomarkers/metabolism ; Metabolomics ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Kidney/metabolism
    Chemical Substances Adenine (JAC85A2161) ; Biomarkers
    Language English
    Publishing date 2023-10-16
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI174015
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  2. Article ; Online: Mechanisms and Implications of Podocyte Autophagy in Chronic Kidney Disease.

    Njeim, Rachel / Merscher, Sandra / Fornoni, Alessia

    American journal of physiology. Renal physiology

    2024  

    Abstract: Autophagy is a protective mechanism through which cells degrade and recycle proteins and organelles to maintain cellular homeostasis and integrity. An accumulating body of evidence underscores the significant impact of dysregulated autophagy on podocyte ... ...

    Abstract Autophagy is a protective mechanism through which cells degrade and recycle proteins and organelles to maintain cellular homeostasis and integrity. An accumulating body of evidence underscores the significant impact of dysregulated autophagy on podocyte injury in chronic kidney disease. In this review, we provide a comprehensive overview of the diverse types of autophagy and their regulation in cellular homeostasis, with a specific emphasis on podocytes. Furthermore, we discuss recent findings that focus on the functional role of different types of autophagy during podocyte injury in chronic kidney disease. The intricate interplay between different types of autophagy and podocyte health requires further research, which is critical for understanding the pathogenesis of CKD and developing targeted therapeutic interventions.
    Language English
    Publishing date 2024-04-11
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00415.2023
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  3. Article ; Online: The Many Lives of PCSK9: Therapeutic Implications.

    Pressly, Jeffrey / Fornoni, Alessia

    Kidney360

    2022  Volume 3, Issue 8, Page(s) 1296–1298

    MeSH term(s) Humans ; Proprotein Convertase 9/genetics ; Proprotein Convertases
    Chemical Substances PCSK9 protein, human (EC 3.4.21.-) ; Proprotein Convertase 9 (EC 3.4.21.-) ; Proprotein Convertases (EC 3.4.21.-)
    Language English
    Publishing date 2022-08-25
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Comment
    ISSN 2641-7650
    ISSN (online) 2641-7650
    DOI 10.34067/KID.0003272022
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  4. Article: Unraveling the Crosstalk between Lipids and NADPH Oxidases in Diabetic Kidney Disease.

    Njeim, Rachel / Alkhansa, Sahar / Fornoni, Alessia

    Pharmaceutics

    2023  Volume 15, Issue 5

    Abstract: Diabetic kidney disease (DKD) is a serious complication of diabetes mellitus and a leading cause of end-stage renal disease. Abnormal lipid metabolism and intrarenal accumulation of lipids have been shown to be strongly correlated with the development ... ...

    Abstract Diabetic kidney disease (DKD) is a serious complication of diabetes mellitus and a leading cause of end-stage renal disease. Abnormal lipid metabolism and intrarenal accumulation of lipids have been shown to be strongly correlated with the development and progression of diabetic kidney disease (DKD). Cholesterol, phospholipids, triglycerides, fatty acids, and sphingolipids are among the lipids that are altered in DKD, and their renal accumulation has been linked to the pathogenesis of the disease. In addition, NADPH oxidase-induced production of reactive oxygen species (ROS) plays a critical role in the development of DKD. Several types of lipids have been found to be tightly linked to NADPH oxidase-induced ROS production. This review aims to explore the interplay between lipids and NADPH oxidases in order to provide new insights into the pathogenesis of DKD and identify more effective targeted therapies for the disease.
    Language English
    Publishing date 2023-04-28
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527217-2
    ISSN 1999-4923
    ISSN 1999-4923
    DOI 10.3390/pharmaceutics15051360
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  5. Article ; Online: Kidney lipid dysmetabolism and lipid droplet accumulation in chronic kidney disease.

    Mitrofanova, Alla / Merscher, Sandra / Fornoni, Alessia

    Nature reviews. Nephrology

    2023  Volume 19, Issue 10, Page(s) 629–645

    Abstract: Chronic kidney disease (CKD) is a global health problem with rising incidence and prevalence. Among several pathogenetic mechanisms responsible for disease progression, lipid accumulation in the kidney parenchyma might drive inflammation and fibrosis, as ...

    Abstract Chronic kidney disease (CKD) is a global health problem with rising incidence and prevalence. Among several pathogenetic mechanisms responsible for disease progression, lipid accumulation in the kidney parenchyma might drive inflammation and fibrosis, as has been described in fatty liver diseases. Lipids and their metabolites have several important structural and functional roles, as they are constituents of cell and organelle membranes, serve as signalling molecules and are used for energy production. However, although lipids can be stored in lipid droplets to maintain lipid homeostasis, lipid accumulation can become pathogenic. Understanding the mechanisms linking kidney parenchymal lipid accumulation to CKD of metabolic or non-metabolic origin is challenging, owing to the tremendous variety of lipid species and their functional diversity across different parenchymal cells. Nonetheless, multiple research reports have begun to emphasize the effect of dysregulated kidney lipid metabolism in CKD progression. For example, altered cholesterol and fatty acid metabolism contribute to glomerular and tubular cell injury. Newly developed lipid-targeting agents are being tested in clinical trials in CKD, raising expectations for further therapeutic development in this field.
    MeSH term(s) Humans ; Lipid Droplets/metabolism ; Lipid Droplets/pathology ; Kidney ; Renal Insufficiency, Chronic/metabolism ; Inflammation/metabolism ; Lipids ; Lipid Metabolism
    Chemical Substances Lipids
    Language English
    Publishing date 2023-07-27
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2490366-8
    ISSN 1759-507X ; 1759-5061
    ISSN (online) 1759-507X
    ISSN 1759-5061
    DOI 10.1038/s41581-023-00741-w
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  6. Article ; Online: Could This Be Alport Syndrome?

    Lennon, Rachel / Fornoni, Alessia

    Clinical journal of the American Society of Nephrology : CJASN

    2021  Volume 16, Issue 11, Page(s) 1743–1745

    MeSH term(s) Adolescent ; Antihypertensive Agents/therapeutic use ; Autoantigens/genetics ; Collagen Type IV/genetics ; Disease Progression ; Genetic Testing ; Humans ; Kidney Transplantation ; Male ; Nephritis, Hereditary/diagnosis ; Nephritis, Hereditary/genetics ; Nephritis, Hereditary/pathology ; Nephritis, Hereditary/therapy
    Chemical Substances Antihypertensive Agents ; Autoantigens ; COL4A5 protein, human ; Collagen Type IV ; type IV collagen alpha3 chain
    Language English
    Publishing date 2021-04-13
    Publishing country United States
    Document type Case Reports ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2226665-3
    ISSN 1555-905X ; 1555-9041
    ISSN (online) 1555-905X
    ISSN 1555-9041
    DOI 10.2215/CJN.00120121
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    Zs.A 6584: Show issues Location:
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  7. Article ; Online: LPCing through the nephron accelerates diabetic kidney disease.

    Pressly, Jeffrey D / Ge, Mengyuan / Fornoni, Alessia

    Kidney international

    2022  Volume 101, Issue 3, Page(s) 454–456

    Abstract: Lipid dysmetabolism is emerging as an important contributor to diabetic kidney disease, suggesting that intrarenal lipid accumulation is detrimental to kidney function. This commentary discusses the finding by Yoshioka et al., connecting tubular ... ...

    Abstract Lipid dysmetabolism is emerging as an important contributor to diabetic kidney disease, suggesting that intrarenal lipid accumulation is detrimental to kidney function. This commentary discusses the finding by Yoshioka et al., connecting tubular lipotoxicity induced by an increase in locally produced lysophosphatidylcholine in patients with a fast progression of diabetic kidney disease, known as "fast decliner." Insight into the lipid species in the kidney may prove beneficial for the diagnosis and stratification of patients with diabetic kidney disease.
    MeSH term(s) Diabetes Mellitus ; Diabetic Nephropathies/etiology ; Humans ; Kidney ; Nephrons
    Language English
    Publishing date 2022-02-19
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2021.12.013
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    Zs.A 797: Show issues Location:
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  8. Article ; Online: Implications of Sphingolipid Metabolites in Kidney Diseases.

    Mallela, Shamroop Kumar / Merscher, Sandra / Fornoni, Alessia

    International journal of molecular sciences

    2022  Volume 23, Issue 8

    Abstract: Sphingolipids, which act as a bioactive signaling molecules, are involved in several cellular processes such as cell survival, proliferation, migration and apoptosis. An imbalance in the levels of sphingolipids can be lethal to cells. Abnormalities in ... ...

    Abstract Sphingolipids, which act as a bioactive signaling molecules, are involved in several cellular processes such as cell survival, proliferation, migration and apoptosis. An imbalance in the levels of sphingolipids can be lethal to cells. Abnormalities in the levels of sphingolipids are associated with several human diseases including kidney diseases. Several studies demonstrate that sphingolipids play an important role in maintaining proper renal function. Sphingolipids can alter the glomerular filtration barrier by affecting the functioning of podocytes, which are key cellular components of the glomerular filtration barrier. This review summarizes the studies in our understanding of the regulation of sphingolipid signaling in kidney diseases, especially in glomerular and tubulointerstitial diseases, and the potential to target sphingolipid pathways in developing therapeutics for the treatment of renal diseases.
    MeSH term(s) Apoptosis ; Female ; Humans ; Kidney Diseases/metabolism ; Male ; Podocytes/metabolism ; Signal Transduction ; Sphingolipids/metabolism
    Chemical Substances Sphingolipids
    Language English
    Publishing date 2022-04-11
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23084244
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  9. Article: Novel Therapies for Alport Syndrome.

    Chavez, Efren / Rodriguez, Juanly / Drexler, Yelena / Fornoni, Alessia

    Frontiers in medicine

    2022  Volume 9, Page(s) 848389

    Abstract: Alport syndrome (AS) is a hereditary kidney disease associated with proteinuria, hematuria and progressive kidney failure. It is characterized by a defective glomerular basement membrane caused by mutations in type IV collagen ... ...

    Abstract Alport syndrome (AS) is a hereditary kidney disease associated with proteinuria, hematuria and progressive kidney failure. It is characterized by a defective glomerular basement membrane caused by mutations in type IV collagen genes
    Language English
    Publishing date 2022-04-25
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2775999-4
    ISSN 2296-858X
    ISSN 2296-858X
    DOI 10.3389/fmed.2022.848389
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  10. Article ; Online: Bedside to bench Alport syndrome research: are human urine-derived podocytes the answer?

    Kim, Jin-Ju / Fornoni, Alessia

    The Journal of pathology

    2020  Volume 253, Issue 1, Page(s) 11–13

    Abstract: In a recent issue of The Journal of Pathology, Iampietro et al isolated and characterized several clones of urine-derived podocytes from three patients with Alport syndrome (AS) and proteinuria and one age-matched non-proteinuric control. They reported ... ...

    Abstract In a recent issue of The Journal of Pathology, Iampietro et al isolated and characterized several clones of urine-derived podocytes from three patients with Alport syndrome (AS) and proteinuria and one age-matched non-proteinuric control. They reported differential expression of genes involved in cell motility, adhesion, survival, and angiogenesis. The authors found AS podocytes to be less motile and to have significantly higher permeability to albumin compared to control podocytes, highlighting that AS podocytes may retain their phenotype even when losing contact with the glomerular basement membrane. The establishment of urine-derived podocyte cell lines from patients with different genetic forms of AS may represent a valuable and minimally invasive tool to investigate the cellular mechanisms contributing to kidney disease progression in AS and may allow for the establishment of patient-specific drug screening opportunities. © 2020 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    MeSH term(s) Glomerular Basement Membrane ; Humans ; Nephritis, Hereditary ; Podocytes ; Proteinuria ; United Kingdom
    Language English
    Publishing date 2020-10-23
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 3119-7
    ISSN 1096-9896 ; 0022-3417
    ISSN (online) 1096-9896
    ISSN 0022-3417
    DOI 10.1002/path.5564
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