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  1. Article ; Online: Urine: from waste to fertilizer.

    Govers, Larissa P / Devuyst, Olivier

    Kidney international

    2022  Volume 102, Issue 6, Page(s) 1206–1208

    MeSH term(s) Fertilizers/adverse effects ; Body Fluids
    Chemical Substances Fertilizers
    Language English
    Publishing date 2022-10-28
    Publishing country United States
    Document type Journal Article
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2022.08.018
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  2. Article: Mitochondrial disease, mitophagy, and cellular distress in methylmalonic acidemia

    Luciani, Alessandro / Denley, Matthew C. S. / Govers, Larissa P. / Sorrentino, Vincenzo / Froese, D. Sean

    Cellular and molecular life sciences. 2021 Nov., v. 78, no. 21-22

    2021  

    Abstract: Mitochondria—the intracellular powerhouse in which nutrients are converted into energy in the form of ATP or heat—are highly dynamic, double-membraned organelles that harness a plethora of cellular functions that sustain energy metabolism and homeostasis. ...

    Abstract Mitochondria—the intracellular powerhouse in which nutrients are converted into energy in the form of ATP or heat—are highly dynamic, double-membraned organelles that harness a plethora of cellular functions that sustain energy metabolism and homeostasis. Exciting new discoveries now indicate that the maintenance of this ever changing and functionally pleiotropic organelle is particularly relevant in terminally differentiated cells that are highly dependent on aerobic metabolism. Given the central role in maintaining metabolic and physiological homeostasis, dysregulation of the mitochondrial network might therefore confer a potentially devastating vulnerability to high-energy requiring cell types, contributing to a broad variety of hereditary and acquired diseases. In this Review, we highlight the biological functions of mitochondria-localized enzymes from the perspective of understanding—and potentially reversing—the pathophysiology of inherited disorders affecting the homeostasis of the mitochondrial network and cellular metabolism. Using methylmalonic acidemia as a paradigm of complex mitochondrial dysfunction, we discuss how mitochondrial directed-signaling circuitries govern the homeostasis and physiology of specialized cell types and how these may be disturbed in disease. This Review also provides a critical analysis of affected tissues, potential molecular mechanisms, and novel cellular and animal models of methylmalonic acidemia which are being used to develop new therapeutic options for this disease. These insights might ultimately lead to new therapeutics, not only for methylmalonic acidemia, but also for other currently intractable mitochondrial diseases, potentially transforming our ability to regulate homeostasis and health.
    Keywords animals ; distress ; energy ; energy metabolism ; homeostasis ; mitochondria ; mitophagy ; pathophysiology ; therapeutics
    Language English
    Dates of publication 2021-11
    Size p. 6851-6867.
    Publishing place Springer International Publishing
    Document type Article
    Note Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-021-03934-3
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: Mitochondrial disease, mitophagy, and cellular distress in methylmalonic acidemia.

    Luciani, Alessandro / Denley, Matthew C S / Govers, Larissa P / Sorrentino, Vincenzo / Froese, D Sean

    Cellular and molecular life sciences : CMLS

    2021  Volume 78, Issue 21-22, Page(s) 6851–6867

    Abstract: Mitochondria-the intracellular powerhouse in which nutrients are converted into energy in the form of ATP or heat-are highly dynamic, double-membraned organelles that harness a plethora of cellular functions that sustain energy metabolism and homeostasis. ...

    Abstract Mitochondria-the intracellular powerhouse in which nutrients are converted into energy in the form of ATP or heat-are highly dynamic, double-membraned organelles that harness a plethora of cellular functions that sustain energy metabolism and homeostasis. Exciting new discoveries now indicate that the maintenance of this ever changing and functionally pleiotropic organelle is particularly relevant in terminally differentiated cells that are highly dependent on aerobic metabolism. Given the central role in maintaining metabolic and physiological homeostasis, dysregulation of the mitochondrial network might therefore confer a potentially devastating vulnerability to high-energy requiring cell types, contributing to a broad variety of hereditary and acquired diseases. In this Review, we highlight the biological functions of mitochondria-localized enzymes from the perspective of understanding-and potentially reversing-the pathophysiology of inherited disorders affecting the homeostasis of the mitochondrial network and cellular metabolism. Using methylmalonic acidemia as a paradigm of complex mitochondrial dysfunction, we discuss how mitochondrial directed-signaling circuitries govern the homeostasis and physiology of specialized cell types and how these may be disturbed in disease. This Review also provides a critical analysis of affected tissues, potential molecular mechanisms, and novel cellular and animal models of methylmalonic acidemia which are being used to develop new therapeutic options for this disease. These insights might ultimately lead to new therapeutics, not only for methylmalonic acidemia, but also for other currently intractable mitochondrial diseases, potentially transforming our ability to regulate homeostasis and health.
    MeSH term(s) Amino Acid Metabolism, Inborn Errors/metabolism ; Animals ; Energy Metabolism/physiology ; Homeostasis/physiology ; Humans ; Mitochondria/metabolism ; Mitochondrial Diseases/metabolism ; Mitophagy/physiology ; Organelles/metabolism ; Signal Transduction/physiology
    Language English
    Publishing date 2021-09-15
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-021-03934-3
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 195: Show issues Location:
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  4. Article ; Online: Mitochondrial DNA mutations in renal disease: an overview.

    Govers, Larissa P / Toka, Hakan R / Hariri, Ali / Walsh, Stephen B / Bockenhauer, Detlef

    Pediatric nephrology (Berlin, Germany)

    2020  Volume 36, Issue 1, Page(s) 9–17

    Abstract: Kidneys have a high energy demand to facilitate the reabsorption of the glomerular filtrate. For this reason, renal cells have a high density of mitochondria. Mitochondrial cytopathies can be the result of a mutation in both mitochondrial and nuclear DNA. ...

    Abstract Kidneys have a high energy demand to facilitate the reabsorption of the glomerular filtrate. For this reason, renal cells have a high density of mitochondria. Mitochondrial cytopathies can be the result of a mutation in both mitochondrial and nuclear DNA. Mitochondrial dysfunction can lead to a variety of renal manifestations. Examples of tubular manifestations are renal Fanconi Syndrome, which is often found in patients diagnosed with Kearns-Sayre and Pearson's marrow-pancreas syndrome, and distal tubulopathies, which result in electrolyte disturbances such as hypomagnesemia. Nephrotic syndrome can be a glomerular manifestation of mitochondrial dysfunction and is typically associated with focal segmental glomerular sclerosis on histology. Tubulointerstitial nephritis can also be seen in mitochondrial cytopathies and may lead to end-stage renal disease. The underlying mechanisms of these cytopathies remain incompletely understood; therefore, current therapies focus mainly on symptom relief. A better understanding of the molecular disease mechanisms is critical in order to improve treatments.
    MeSH term(s) DNA, Mitochondrial/genetics ; Humans ; Kearns-Sayre Syndrome ; Mitochondria/genetics ; Mitochondrial Myopathies ; Mutation ; Nephritis, Interstitial
    Chemical Substances DNA, Mitochondrial
    Language English
    Publishing date 2020-01-10
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-019-04404-6
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  5. Article ; Online: Modeling the Accumulation of Degradable Polymer Drug Carriers in the Brain.

    Bolwerk, Celine / Govers, Larissa P M W D / Knol, Hanna / Oostendorp, Thom F / Brock, Roland

    ChemMedChem

    2018  Volume 13, Issue 13, Page(s) 1308–1310

    Abstract: The blood-brain barrier (BBB) limits the access of drugs to the brain. Intensive research is being conducted on the development of nanoparticulate drug carriers that mediate transfer across the BBB. A question that has been neglected so far is the ... ...

    Abstract The blood-brain barrier (BBB) limits the access of drugs to the brain. Intensive research is being conducted on the development of nanoparticulate drug carriers that mediate transfer across the BBB. A question that has been neglected so far is the potential accumulation of the carrier in the brain upon long-term exposure. Here, we address this question by implementing a kinetic model to relate drug loading, required concentration of drug in the brain, and drug clearance to the degradation half-life of the carrier. As a test case with clinical relevance we chose poly-lactic-co-glycolic-acid (PLGA) as a carrier material and a chemotherapeutic for which the required parameters could be recovered from the literature. For methotrexate with a drug load of 8.5 %, a required concentration of free drug of 1 μm, a release from PLGA of 6 hours, a drug clearance from the brain of 3 hours and a half-life of polymer degradation of 28 days, a steady-state accumulation of 1.3 g polymer would be reached in the brain (1.5 L) after seven months. While this number is surprisingly small, further physiological research is warranted to assess to which degree this will be in a tolerable range.
    MeSH term(s) Blood-Brain Barrier/metabolism ; Drug Carriers/chemistry ; Drug Carriers/pharmacokinetics ; Drug Liberation ; Half-Life ; Kinetics ; Metabolic Clearance Rate ; Methotrexate/chemistry ; Methotrexate/pharmacokinetics ; Models, Biological ; Nanoparticles/chemistry ; Polylactic Acid-Polyglycolic Acid Copolymer/chemistry ; Polylactic Acid-Polyglycolic Acid Copolymer/pharmacokinetics
    Chemical Substances Drug Carriers ; Polylactic Acid-Polyglycolic Acid Copolymer (1SIA8062RS) ; Methotrexate (YL5FZ2Y5U1)
    Language English
    Publishing date 2018-06-10
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 2218496-X
    ISSN 1860-7187 ; 1860-7179
    ISSN (online) 1860-7187
    ISSN 1860-7179
    DOI 10.1002/cmdc.201800186
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    Zs.A 6280: Show issues Location:
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  6. Article ; Online: Low plasma magnesium concentration and future abdominal aortic calcifications in moderate chronic kidney disease.

    Ter Braake, Anique D / Govers, Larissa P / Peeters, Mieke J / van Zuilen, Arjan D / Wetzels, Jack F M / Blankenstijn, Peter J / Hoenderop, Joost G J / de Baaij, Jeroen H F / van den Brand, Jan A J G

    BMC nephrology

    2021  Volume 22, Issue 1, Page(s) 71

    Abstract: Background: Higher plasma magnesium concentrations are associated with reduced cardiovascular disease risk in chronic kidney disease (CKD) patients. The importance of plasma magnesium concentration for vascular calcification in earlier stages of CKD ... ...

    Abstract Background: Higher plasma magnesium concentrations are associated with reduced cardiovascular disease risk in chronic kidney disease (CKD) patients. The importance of plasma magnesium concentration for vascular calcification in earlier stages of CKD remains underexplored. This study investigated whether plasma magnesium is a determinant for the presence and severity of vascular calcification in moderate CKD.
    Methods: Retrospective analysis was performed using abdominal aortic calcification (AAC) scores in 280 patients with stage 3 and 4 CKD enrolled in the MASTERPLAN trial. Lateral abdominal X-ray was used to evaluate AAC. Plasma magnesium concentration were measured over time. A zero-inflated Poisson model determined the association between plasma magnesium concentration and AAC.
    Results: 79 out of 280 patients did not have AAC, and in patients with AAC the median calcification score was 3.5 (interquartile range: 0.0-8.6). The mean plasma magnesium concentration was 0.76 ± 0.10 mmol/L at baseline. A 0.1 mmol/L higher plasma magnesium concentration was associated with lower AAC of 0.07 point (95% CI -0.28 - 0.14). A 0.1 mmol/L higher plasma magnesium lowered the odds of detecting any AAC by 30% (OR = 0.63; 95% CI 0.29-1.37). After 1 year and 4 years (at time of X-ray) of follow-up this association was attenuated (OR = 0.93; 95% CI 0.61-1.43 and 0.93; 95% CI 0.60-1.45, respectively). None of these associations reached statistical significance.
    Conclusions: Plasma magnesium concentration at baseline is not associated with the risk for future AAC. Interventions increasing magnesium to avoid vascular calcification may have greatest potential in early CKD stages prior to onset of vascular calcification.
    MeSH term(s) Adult ; Aged ; Aorta, Abdominal ; Aortic Diseases/etiology ; Female ; Humans ; Magnesium/blood ; Male ; Middle Aged ; Renal Insufficiency, Chronic/blood ; Renal Insufficiency, Chronic/complications ; Retrospective Studies ; Severity of Illness Index ; Vascular Calcification/etiology
    Chemical Substances Magnesium (I38ZP9992A)
    Language English
    Publishing date 2021-02-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2041348-8
    ISSN 1471-2369 ; 1471-2369
    ISSN (online) 1471-2369
    ISSN 1471-2369
    DOI 10.1186/s12882-021-02267-4
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  7. Article ; Online: Organic anion transporters 1 and 3 influence cellular energy metabolism in renal proximal tubule cells.

    Vriend, Jelle / Hoogstraten, Charlotte A / Venrooij, Kevin R / van den Berge, Bartholomeus T / Govers, Larissa P / van Rooij, Arno / Huigen, Marleen C D G / Schirris, Tom J J / Russel, Frans G M / Masereeuw, Rosalinde / Wilmer, Martijn J

    Biological chemistry

    2019  Volume 400, Issue 10, Page(s) 1347–1358

    Abstract: Organic anion transporters (OATs) 1 and 3 are, besides being uptake transporters, key in several cellular metabolic pathways. The underlying mechanisms are largely unknown. Hence, we used human conditionally immortalized proximal tubule epithelial cells ( ...

    Abstract Organic anion transporters (OATs) 1 and 3 are, besides being uptake transporters, key in several cellular metabolic pathways. The underlying mechanisms are largely unknown. Hence, we used human conditionally immortalized proximal tubule epithelial cells (ciPTEC) overexpressing OAT1 or OAT3 to gain insight into these mechanisms. In ciPTEC-OAT1 and -OAT3, extracellular lactate levels were decreased (by 77% and 71%, respectively), while intracellular ATP levels remained unchanged, suggesting a shift towards an oxidative phenotype upon OAT1 or OAT3 overexpression. This was confirmed by increased respiration of ciPTEC-OAT1 and -OAT3 (1.4-fold), a decreased sensitivity to respiratory inhibition, and characterized by a higher demand on mitochondrial oxidative capacity. In-depth profiling of tricarboxylic acid (TCA) cycle metabolites revealed reduced levels of intermediates converging into α-ketoglutarate in ciPTEC-OAT1 and -OAT3, which via 2-hydroxyglutarate metabolism explains the increased respiration. These interactions with TCA cycle metabolites were in agreement with metabolomic network modeling studies published earlier. Further studies using OAT or oxidative phosphorylation (OXPHOS) inhibitors confirmed our idea that OATs are responsible for increased use and synthesis of α-ketoglutarate. In conclusion, our results indicate an increased α-ketoglutarate efflux by OAT1 and OAT3, resulting in a metabolic shift towards an oxidative phenotype.
    MeSH term(s) Energy Metabolism ; HEK293 Cells ; Humans ; Ketoglutaric Acids/metabolism ; Kidney Tubules, Proximal/metabolism ; Organic Anion Transport Protein 1/metabolism ; Organic Anion Transporters, Sodium-Independent/metabolism
    Chemical Substances Ketoglutaric Acids ; Organic Anion Transport Protein 1 ; Organic Anion Transporters, Sodium-Independent ; organic anion transport protein 3
    Language English
    Publishing date 2019-01-16
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1334659-3
    ISSN 1437-4315 ; 1431-6730 ; 1432-0355
    ISSN (online) 1437-4315
    ISSN 1431-6730 ; 1432-0355
    DOI 10.1515/hsz-2018-0446
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