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Mitochondria Damage and Kidney Disease

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Book cover Mitochondrial Dynamics in Cardiovascular Medicine

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 982))

Abstract

The kidney is a vital organ that demands an extraordinary amount of energy to actively maintain the body’s metabolism, plasma hemodynamics, electrolytes and water homeostasis, nutrients reabsorption, and hormone secretion. Kidney is only second to the heart in mitochondrial count and oxygen consumption. As such, the health and status of the energy power house, the mitochondria, is pivotal to the health and proper function of the kidney. Mitochondria are heterogeneous and highly dynamic organelles and their functions are subject to complex regulations through modulation of its biogenesis, bioenergetics, dynamics and clearance within cell. Kidney diseases, either acute kidney injury (AKI) or chronic kidney disease (CKD), are important clinical issues and global public health concerns with high mortality rate and socioeconomic burden due to lack of effective therapeutic strategies to cure or retard the progression of the diseases. Mitochondria-targeted therapeutics has become a major focus for modern research with the belief that maintaining mitochondria homeostasis can prevent kidney pathogenesis and disease progression. A better understanding of the cellular and molecular events that govern mitochondria functions in health and disease will potentially lead to improved therapeutics development.

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Abbreviations

AKI:

Acute kidney injury

AMPK:

AMP-activated protein kinase

ATP:

Adenosine triphosphate

Ca2+ :

Calcium ion

CKD:

Chronic kidney disease

coQ:

Coenzyme Q

CsA:

Cyclosporin A

cyt C:

Cytochrome C

DN:

Diabetic nephropathy

dNTPs:

Deoxynucleotides triphosphates

DRP1:

Dynamin related protein 1

ESRD:

End-stage renal disease

ETC:

Electron transport chain

FSGS:

Focal and segmental glomerulosclerosis

GN:

Glomerulonephritis

GSK:

Glycogen synthase kinase

H+ :

Proton

I/R injury or IRI:

Ischemic reperfusion injury

IMM:

Inner mitochondrial membrane

KLF-6:

Krüppel-like factor 6

MELAS:

Myopathy encephalopathy lactic acidosis and stroke-like episodes

Mfn1 and 2:

Mitofusins 1 and 2

MPT:

Mitochondrial permeability transition

mPTP:

Mitochondrial permeability transition pore

mtDNA:

Mitochondrial DNA

MA-5:

Mitochonic acid 5

NAD+ :

Nicotinamide adenine dinucleotide

nDNA:

Nuclear DNA

NRF:

Nuclear respiratory factors

OMM:

Outer mitochondrial membrane

OPA1:

Optical atrophy 1

OXPHOS:

Oxidative phosphorylation

PGC-1α:

PPARγ-coactivator -1α

PPAR:

Peroxisome proliferator-activated receptor

ROS:

Reactive oxygen species

SIRT:

Sirtuin

TLR:

Toll-like receptor

ΔΨm:

Mitochondrial inner membrane potential

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Acknowledgments

PHL is supported, in part, by an OSU intramural Lockwood Fund.

Conflict of Interest

No competing interest.

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Authors and Affiliations

  1. Department of Surgery, Baylor College of Medicine, Houston, TX, 77030, USA

    Pu Duann

  2. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, 43210, USA

    Pei-Hui Lin

  3. Department of Surgery, The Ohio State University, Columbus, OH, 43210, USA

    Pei-Hui Lin

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  1. Pu Duann
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  2. Pei-Hui Lin
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Correspondence to Pu Duann or Pei-Hui Lin .

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Editors and Affiliations

  1. Dept. of Biomedical Advanced Sciences, Federico II University, Naples, Italy

    Gaetano Santulli

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Duann, P., Lin, PH. (2017). Mitochondria Damage and Kidney Disease. In: Santulli, G. (eds) Mitochondrial Dynamics in Cardiovascular Medicine. Advances in Experimental Medicine and Biology, vol 982. Springer, Cham. https://doi.org/10.1007/978-3-319-55330-6_27

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