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. 2022 May 10;11(10):1598. doi: 10.3390/cells11101598

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Effect of sepsis on mitochondrial oxidative phosphorylation and compensatory mechanisms for restoring oxidative phosphorylation efficiency (A) Interaction between bacterial lipopolysaccharide (LPS) and toll-like receptors (TLRs) induces pro inflammatory cytokines and triggers radical oxygen species (ROS) and nitric oxide (NO) generation. Increased in ROS and NO production cause damage to ETC components and ATP synthase, and induces a loss of membrane potential through the activation of mitochondrial permeability transition pores (mPTP). Activation of UCP 2 dissipates ROS production but it is not strong enough to prevent the uncoupling of oxidative phosphorylation. (B) Predicted consequences of damage to ETC components and ATP synthase in mitochondrial respiration, and ATP generation and ROS production across the time course of sepsis. (C) Time course of the response of mitochondrial bioenergetic and biogenesis parameters to sepsis, and the expected changes in the coupling efficiency in the recovery phase of sepsis, according to the current knowledge. Arrow () indicate increase, arrow () indicate decrease, arrow () indicate no changes.

Inline graphic — Effect of sepsis on mitochondrial oxidative phosphorylation and compensatory mechanisms for restoring oxidative phosphorylation efficiency (A) Interaction between bacterial lipopolysaccharide (LPS) and toll-like receptors (TLRs) induces pro inflammatory cytokines and triggers radical oxygen species (ROS) and nitric oxide (NO) generation. Increased in ROS and NO production cause damage to ETC components and ATP synthase, and induces a loss of membrane potential through the activation of mitochondrial permeability transition pores (mPTP). Activation of UCP 2 dissipates ROS production but it is not strong enough to prevent the uncoupling of oxidative phosphorylation. (B) Predicted consequences of damage to ETC components and ATP synthase in mitochondrial respiration, and ATP generation and ROS production across the time course of sepsis. (C) Time course of the response of mitochondrial bioenergetic and biogenesis parameters to sepsis, and the expected changes in the coupling efficiency in the recovery phase of sepsis, according to the current knowledge. Arrow () indicate increase, arrow () indicate decrease, arrow () indicate no changes.