Mitochondrial energetics in the kidney

Latest Reviews

  • Review |

    CD36 has important roles in lipid homeostasis, metabolic inflammation, reprogramming of energy metabolism, apoptosis and kidney fibrosis. Here, the authors discuss these roles as well as the regulation and post-translational modification of CD36 and its potential as a biomarker and a therapeutic target for kidney disease.

    • Xiaochun Yang
    • , Daryl M. Okamura
    • , Xifeng Lu
    • , Yaxi Chen
    • , John Moorhead
    • , Zac Varghese
    •  & Xiong Z. Ruan
  • Review |

    Cardiac surgery-associated acute kidney injury (CSA-AKI) is the most common complication in adult patients undergoing open heart surgery. In this Review, the authors discuss the definition, epidemiology, pathophysiology and risk factors of CSA-AKI. The authors also explore the use of novel biomarkers of AKI and their potential utility in preventing or treating CSA-AKI.

    • Ying Wang
    •  & Rinaldo Bellomo
  • Review |

    The incretin hormone glucagon-like peptide 1 (GLP-1) has been implicated in the gut–renal axis and incretin-based therapies might reduce the burden of diabetic kidney disease. Here, the authors review the physiological roles of GLP-1, the potential renoprotective mechanisms of incretin-based therapies and the available renal outcome data from clinical trials.

    • Marcel H. A. Muskiet
    • , Lennart Tonneijck
    • , Mark M. Smits
    • , Michaël J.B. van Baar
    • , Mark H. H. Kramer
    • , Ewout J. Hoorn
    • , Jaap A. Joles
    •  & Daniël H. van Raalte
  • Review |

    Mitochondria provide the kidney with energy to remove waste from the blood and regulate fluid and electrolyte balance. This Review discusses how mitochondrial homeostasis is maintained, the changes in mitochondrial energetics that occur in acute kidney injury and diabetic nephropathy, and how targeting mitochondrial energetics might aid the treatment of renal disease.

    • Pallavi Bhargava
    •  & Rick G. Schnellmann
  • Review |

    Uromodulin is the most abundant urinary protein. Here, the authors discuss the physiological roles of uromodulin, the mechanisms by which mutations in the UMOD gene, which encodes uromodulin, cause autosomal dominant tubulointerstitial kidney disease and the association of common UMOD variants with complex disorders in the general population.

    • Olivier Devuyst
    • , Eric Olinger
    •  & Luca Rampoldi
  • Review |

    A growing body of evidence supports a key role for T helper type 17 (TH17) cells in the development of renal damage. This Review discusses the identification, regulation, and function of TH17 cells and their associated pathways in immune-mediated kidney diseases, with particular focus on the mechanisms underlying renal tissue injury.

    • Christian F. Krebs
    • , Tilman Schmidt
    • , Jan-Hendrik Riedel
    •  & Ulf Panzer

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