Mitochondrial energetics in the kidney
Reads0
Chats0
TLDR
Implementing compounds that stimulate mitochondrial biogenesis can restore mitochondrial and renal function in mouse models of AKI and diabetes mellitus and inhibiting the fission protein dynamin 1-like protein (DRP1) might ameliorate ischaemic renal injury by blocking mitochondrial fission.Abstract:
The kidney requires a large number of mitochondria to remove waste from the blood and regulate fluid and electrolyte balance. Mitochondria provide the energy to drive these important functions and can adapt to different metabolic conditions through a number of signalling pathways (for example, mechanistic target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK) pathways) that activate the transcriptional co-activator peroxisome proliferator-activated receptor-γ co-activator 1α (PGC1α), and by balancing mitochondrial dynamics and energetics to maintain mitochondrial homeostasis. Mitochondrial dysfunction leads to a decrease in ATP production, alterations in cellular functions and structure, and the loss of renal function. Persistent mitochondrial dysfunction has a role in the early stages and progression of renal diseases, such as acute kidney injury (AKI) and diabetic nephropathy, as it disrupts mitochondrial homeostasis and thus normal kidney function. Improving mitochondrial homeostasis and function has the potential to restore renal function, and administering compounds that stimulate mitochondrial biogenesis can restore mitochondrial and renal function in mouse models of AKI and diabetes mellitus. Furthermore, inhibiting the fission protein dynamin 1-like protein (DRP1) might ameliorate ischaemic renal injury by blocking mitochondrial fission.read more
Citations
More filters
Journal ArticleDOI
A novel hypothesis linking low-grade ketonaemia to cardio-renal benefits with sodium-glucose cotransporter-2 inhibitors.
TL;DR: In this article, the authors proposed a novel hypothesis to link the pleiotropic effects of low-grade ketonaemia to the cardio-renal benefits seen with SGLT2 inhibitors.
Journal ArticleDOI
Relationship between renal capacity to reabsorb glucose and renal status in patients with diabetes
Odette Matar,Louis Potier,Yawa Abouleka,M. Hallot-Feron,Frédéric Fumeron,Kamel Mohammedi,Samy Hadjadj,Ronan Roussel,Gilberto Velho,Michel Marre +9 more
TL;DR: High glucose reabsorption capacity in renal proximal tubules is associated with high UAE and low eGFR in patients with diabetes and blood glucose levels > 11 mmol/L in patients in the high blood glucose group.
Journal ArticleDOI
A transcriptional metastatic signature predicts survival in clear cell renal cell carcinoma
Adele M. Alchahin,Shenglin Mei,Ioanna Tsea,Taghreed Hirz,Youmna Kfoury,Douglas M. Dahl,Chin-Lee Wu,Alexander O. Subtelny,Shulin Wu,David T. Scadden,John H. Shin,Philip J. Saylor,David B. Sykes,Peter V. Kharchenko,Ninib Baryawno +14 more
TL;DR: In this paper , a cell-to-cell interaction analysis highlights the CXCL9/CXCL10-CXCR3 axis and the CD70-CD27 axis as potential therapeutic targets.
Posted ContentDOI
Towards Building a Smart Kidney Atlas: Network-based integration of multimodal transcriptomic, proteomic, metabolomic and imaging data in the Kidney Precision Medicine Project
Jens Hansen,Rachel Sealfon,Rajasree Menon,Michael T. Eadon,Blue B. Lake,Becky Steck,Dejan Dobi,Samir M. Parikh,Tara K. Sidgel,Theodore Alexandrov,Andrew Schroeder,Edgar A. Otto,Christopher R. Anderton,Christopher R. Anderton,Daria Barwinska,Guanshi Zheng,Michael Rose,John P. Shapiro,Dušan Veličković,Annapurna Pamreddy,Seth Winfree,Yongqun He,Ian H. de Boer,Jeffrey B. Hodgin,Abhijit Nair,Kumar Sharma,Minnie M. Sarwal,Kun Zhang,Jonathan Himmelfarb,Zoltan Laszik,Brad H. Rovin,Pierre C. Dagher,John Cijiang He,Tarek M. El-Achkar,Sanjay Jain,Olga G. Troyanskaya,Matthias Kretzler,Ravi Iyengar,Evren U. Azeloglu +38 more
TL;DR: A set of hierarchical analytical methods to process, combine, and harmonize single-cell, single-nucleus and subsegmental laser microdissection (LMD) transcriptomics and 3-D nondestructive and immunofluorescence-based Codex imaging and spatial metabolomics datasets are described.
Journal ArticleDOI
Exendin-4 Improves Diabetic Kidney Disease in C57BL/6 Mice Independent of Brown Adipose Tissue Activation.
Shu Fang,Yingying Cai,Yingying Cai,Fuping Lyu,Fuping Lyu,Hongbin Zhang,Chunyan Wu,Yanmei Zeng,Cunxia Fan,Shaozhou Zou,Yudan Zhang,Ping Li,Ling Wang,YaomingXue,Meiping Guan +14 more
TL;DR: Exendin-4 could decrease the renal lipid deposit and improve diabetic nephropathy via activating the renal AMPK pathway independent of BAT activation in diabetic mice regardless of BAT excision.
References
More filters
Journal ArticleDOI
Biochemistry and molecular cell biology of diabetic complications
TL;DR: This integrating paradigm provides a new conceptual framework for future research and drug discovery in diabetes-specific microvascular disease and seems to reflect a single hyperglycaemia-induced process of overproduction of superoxide by the mitochondrial electron-transport chain.
Book
Molecular Cell Biology
TL;DR: Molecular cell biology, Molecular cell biology , مرکز فناوری اطلاعات و اصاع رسانی, کδاوρزی
Journal ArticleDOI
Targeting HIF-1 for cancer therapy
TL;DR: Hypoxia-inducible factor 1 (HIF-1) activates the transcription of genes that are involved in crucial aspects of cancer biology, including angiogenesis, cell survival, glucose metabolism and invasion.
Journal ArticleDOI
Oxidative stress and diabetic complications
TL;DR: Athrosclerosis and cardiomyopathy in type 2 diabetes are caused in part by pathway-selective insulin resistance, which increases mitochondrial ROS production from free fatty acids and by inactivation of antiatherosclerosis enzymes by ROS.
Journal ArticleDOI
Mechanisms Controlling Mitochondrial Biogenesis and Respiration through the Thermogenic Coactivator PGC-1
Zhidan Wu,Pere Puigserver,Ulf Andersson,Chen-Yu Zhang,Guillaume Adelmant,Vamsi K. Mootha,Amy E Troy,Saverio Cinti,Bradford B. Lowell,Richard C. Scarpulla,Bruce M. Spiegelman +10 more
TL;DR: PGC-1, a cold-inducible coactivator of nuclear receptors, stimulates mitochondrial biogenesis and respiration in muscle cells through an induction of uncoupling protein 2 (UCP-2) and through regulation of the nuclear respiratory factors (NRFs).