Biochemistry (Moscow)

, Volume 77, Issue 7, pp 742–753

The phenoptosis problem: What is causing the death of an organism? Lessons from acute kidney injury

Authors

    • Belozersky Institute of Physico-Chemical BiologyLomonosov Moscow State University
    • Institute of MitoengineeringLomonosov Moscow State University
  • E. Y. Plotnikov
    • Belozersky Institute of Physico-Chemical BiologyLomonosov Moscow State University
    • Institute of MitoengineeringLomonosov Moscow State University
  • S. S. Jankauskas
    • Institute of MitoengineeringLomonosov Moscow State University
    • Faculty of Bioengineering and BioinformaticsLomonosov Moscow State University
  • N. K. Isaev
    • Belozersky Institute of Physico-Chemical BiologyLomonosov Moscow State University
    • Institute of MitoengineeringLomonosov Moscow State University
  • D. N. Silachev
    • Belozersky Institute of Physico-Chemical BiologyLomonosov Moscow State University
    • Institute of MitoengineeringLomonosov Moscow State University
  • L. D. Zorova
    • Institute of MitoengineeringLomonosov Moscow State University
    • International Laser CenterLomonosov Moscow State University
  • I. B. Pevzner
    • Institute of MitoengineeringLomonosov Moscow State University
    • Faculty of Bioengineering and BioinformaticsLomonosov Moscow State University
  • N. V. Pulkova
    • Institute of MitoengineeringLomonosov Moscow State University
    • Faculty of Bioengineering and BioinformaticsLomonosov Moscow State University
  • S. D. Zorov
    • Institute of MitoengineeringLomonosov Moscow State University
    • Faculty of Bioengineering and BioinformaticsLomonosov Moscow State University
  • M. A. Morosanova
    • Institute of MitoengineeringLomonosov Moscow State University
    • Faculty of Bioengineering and BioinformaticsLomonosov Moscow State University
Review

DOI: 10.1134/S0006297912070073

Cite this article as:
Zorov, D.B., Plotnikov, E.Y., Jankauskas, S.S. et al. Biochemistry Moscow (2012) 77: 742. doi:10.1134/S0006297912070073

Abstract

Programmed execution of various cells and intracellular structures is hypothesized to be not the only example of elimination of biological systems — the general mechanism can also involve programmed execution of organs and organisms. Modern rating of programmed cell death mechanisms includes 13 mechanistic types. As for some types, the mechanism of actuation and manifestation of cell execution has been basically elucidated, while the causes and intermediate steps of the process of fatal failure of organs and organisms remain unknown. The analysis of deaths resulting from a sudden heart arrest or multiple organ failure and other acute and chronic pathologies leads to the conclusion of a special role of mitochondria and oxidative stress activating the immune system. Possible mechanisms of mitochondria-mediated induction of the signaling cascades involved in organ failure and death of the organism are discussed. These mechanisms include generation of reactive oxygen species and damage-associated molecular patterns in mitochondria. Some examples of renal failure-induced deaths are presented with mechanisms and settings determined by some hypothetical super system rather than by the kidneys themselves. This system plays the key role in the process of physiological senescence and termination of an organism. The facts presented suggest that it is the immune system involved in mitochondrial signaling that can act as the system responsible for the organism’s death.

Key words

sudden deathmultiple organ failureapoptosiskidneymitochondriaantioxidant

Abbreviations

AIF

apoptosis-inducing factor

DAMP

damage-associated molecular patterns

MODS

multiple organ dysfunction syndrome

mtDNA

mitochondrial DNA

PAMP

pathogen-associated molecular patterns

PARP

poly(ADP-ribose) polymerase

ROS

reactive oxygen species

SCA

sudden cardiac arrest

SkQ1

10-(6′-plastoquinonyl) decyltriphenylphosphonium

SkQR1

10-(6′-plastoquinonyl) decylrhodamine 19

Copyright information

© Pleiades Publishing, Ltd. 2012