The Potential Mechanism of D-Amino Acids – Mitochondria Axis in the Progression of Diabetic Kidney Disease
Diabetic kidney disease (DKD) is a major complication of diabetes mellitus (DM) and stands out as the leading cause of end-stage renal disease worldwide. There is increasing evidence that mitochondrial dysfunction, including impaired mitochondrial biogenesis, dynamics, and oxidative stress, contribu...
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Published in | Kidney international reports Vol. 10; no. 2; pp. 343 - 354 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.02.2025
Elsevier |
Subjects | |
Online Access | Get full text |
ISSN | 2468-0249 2468-0249 |
DOI | 10.1016/j.ekir.2024.11.008 |
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Summary: | Diabetic kidney disease (DKD) is a major complication of diabetes mellitus (DM) and stands out as the leading cause of end-stage renal disease worldwide. There is increasing evidence that mitochondrial dysfunction, including impaired mitochondrial biogenesis, dynamics, and oxidative stress, contributes to the development and progression of DKD. D-amino acids (D-AAs), which are enantiomers of L-AAs, have recently been detected in various living organisms and are acknowledged to play important roles in numerous physiological processes in the human body. Accumulating evidence demonstrates that D-AA levels in blood or urine could serve as useful biomarkers for reflecting renal function. The physiological roles of D-AAs are implicated in the regulation of cellular proliferation, oxidative stress, generation of reactive oxygen species (ROS), and innate immunity. This article reviews current evidence relating to D-AAs and mitochondrial dysfunction and proposes a potential interaction and contribution of the D-AAs–mitochondria axis in DKD pathophysiology and progression. This insight could provide novel therapeutic approaches for preventing or ameliorating DKD based on this biological axis. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 |
ISSN: | 2468-0249 2468-0249 |
DOI: | 10.1016/j.ekir.2024.11.008 |