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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Published on: January 7, 2013

Mitochondrial Alterations and CKD.

Jairo A Pinzon-Cortes¹, Phoom Narongkiatikhun², Long Yuan³

¹Department of Medicine, Division of Endocrinology, Metabolism and Nutrition, University of Washington School of Medicine, Seattle, WA, USA; Diabetes Department, School of Translational Medicine, Monash University, Melbourne, VIC, Australia.

American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation

|June 22, 2026

Summary

This summary is machine-generated.

Mitochondrial dysfunction drives chronic kidney disease (CKD) progression. Targeting these cellular powerhouses with novel therapies offers a promising strategy to improve kidney health and patient outcomes.

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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

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Published on: January 7, 2013

Using Live Cell STED Imaging to Visualize Mitochondrial Inner Membrane Ultrastructure in Neuronal Cell Models

Using Live Cell STED Imaging to Visualize Mitochondrial Inner Membrane Ultrastructure in Neuronal Cell Models

Published on: June 30, 2023

Area of Science:

Nephrology
Mitochondrial Biology
Cellular Metabolism

Background:

Mitochondrial alterations are key in chronic kidney disease (CKD) pathogenesis.
These changes impact energy metabolism, oxidative stress, and cellular responses in both diabetic and non-diabetic CKD.
Understanding mitochondrial remodeling is crucial for developing effective treatments.

Purpose of the Study:

To review recent advances in understanding mitochondrial remodeling in CKD.
To highlight state-of-the-art methods for assessing mitochondrial health.
To discuss therapeutic strategies targeting mitochondrial pathways in CKD.

Main Methods:

Review of current literature on mitochondrial alterations in CKD.
Discussion of advanced assessment techniques: high-resolution respirometry, metabolomics, transcriptomics, functional MRI, and PET imaging.
Analysis of therapeutic agents modulating mitochondrial function.

Main Results:

Mitochondrial remodeling involves changes in bioenergetics, dynamics, redox balance, and biogenesis in CKD.
Various advanced techniques enable comprehensive assessment of mitochondrial health.
Several therapeutic agents (e.g., SGLT2 inhibitors, GLP-1 agonists, nsMRAs, NAD+ boosters) show promise.

Conclusions:

Targeting mitochondrial adaptation is a compelling therapeutic strategy for CKD.
Precision phenotyping using multi-omics and spatial profiling can guide individualized therapy.
Improving mitochondrial health holds potential to enhance outcomes in patients with CKD.