Renal Failure

Kidneys are highly active organs that not only remove waste but regulate salt-water balance, electrolyte homeostasis, blood pressure, the number of red blood cells and vitamin D level. The high metabolic activity demands high energy production and at the same time, a controlled production of reactive oxygen species necessary for normal cellular signaling. Kidney cellular metabolism is supported by both mitochondrial bioenergetics and glycolysis. The metabolic pathways utilized are different in various parts of the nephron. In rapidly dividing cells, mitochondrial function is partially suppressed whereas glycolysis is upregulated to provide biomass for newly synthesized molecules. ATP synthesis in mitochondria occurs through a process called oxidative phosphorylation. Mitochondria are also involved in calcium and iron homeostasis and are the main cellular source of reactive oxygen species that regulate cell survival and death.

Mitochondrial dysfunction has been proposed to be either a cause or a consequence in kidney pathophysiology. Because of the limited regenerative capability of the kidney, an imbalance of these functions makes it vulnerable to diseases. A better understanding of mechanisms underlying mitochondrial adaptation or dysfunction during the pathogenesis of the various kidney diseases may lead to improved diagnosis and novel therapies. Pharmacological manipulation of mitochondrial metabolism and cellular bioenergetics to preserve renal function, or revert damages caused by metabolic imbalance, became a topic of high interest in recent years.

This special announcement aims to provide a collection of articles relevant to renal mitochondrial bioenergetics and mitochondrial metabolism. Contributions that present new hypotheses, novel observations, analyze mitochondrial dysfunction in renal diseases or propose novel drug developments are of interest.

Subtopics included are: Mitochondrial dysfunction in

1. Acute renal diseases;

2. Kidney transplant;

3. Chronic renal diseases including diabetic renal disease;

4. Mitochondrial bioenergetics in genetic renal diseases;

5. Age-related changes in mitochondrial metabolism in the kidney.

All article types that are in the scope of the Journal are welcome.

Keywords: bioenergetics, mitochondrial redox state, mitochondrial biogenesis, kidney failure, mitochondrial dynamics

Monika Gooz, M.D. Ph.D. is an Associate Professor at the Department of Drug Discovery and Biomedical Sciences and a Chan Zuckerberg Imaging Scientist at the Cell and Molecular Imaging Core as well as the Drug Discovery Core at the College of Pharmacy of the Medical University of South Carolina (MUSC), Charleston, SC. She has extensive experience in the use of advanced imaging approaches for visualization of protein interactions and metabolic changes in several cellular and animal models including polycystic kidney diseases and cancer.

Eduardo N. Maldonado, DVM, Ph.D. is an Associate Professor at the Department of Drug Discovery and Biomedical Sciences at the Medical University of South Carolina (MUSC), Charleston, SC. His main research focus is the study of mitochondrial metabolism and cellular bioenergetics in cancer and other diseases. His research aims to understand the biology of mitochondrial function and to identify potential mechanisms that could be used to develop drugs that modify cellular metabolism.

Disclosure Statement: Prof. Gooz and Prof. Maldonado declare there is no conflict of interest.

Instructions for AuthorsSubmit an Article