Mitochondrial control of inflammation

Abstract

Numerous mitochondrial constituents and metabolic products can function as damage-associated molecular patterns (DAMPs) and promote inflammation when released into the cytosol or extracellular milieu. Several safeguards are normally in place to prevent mitochondria from eliciting detrimental inflammatory reactions, including the autophagic disposal of permeabilized mitochondria. However, when the homeostatic capacity of such systems is exceeded or when such systems are defective, inflammatory reactions elicited by mitochondria can become pathogenic and contribute to the aetiology of human disorders linked to autoreactivity. In addition, inefficient inflammatory pathways induced by mitochondrial DAMPs can be pathogenic as they enable the establishment or progression of infectious and neoplastic disorders. Here we discuss the molecular mechanisms through which mitochondria control inflammatory responses, the cellular pathways that are in place to control mitochondria-driven inflammation and the pathological consequences of dysregulated inflammatory reactions elicited by mitochondrial DAMPs.

Epigallocatechin-3-gallate Mo nanoparticles (EGM NPs) efficiently treat liver injury by strongly reducing oxidative stress, inflammation and endoplasmic reticulum stress

“…NAPQI directly interferes with ETC, resulting in the massive production of ROS. Mitochondria are the major source of intracellular ROS and play a key role in the production of ATP, the regulation of various catabolic and anabolic processes, and the maintenance of redox homeostasis (Bonora et al, 2022;Marchi et al, 2022). Under normal physiological conditions, ETC produces ROS as a by-product during oxidative phosphorylation process.…”

Mitochondrial oxidative stress in the tumor microenvironment and cancer immunoescape: foe or friend?

“…It is generally accepted that the TME is a chronic inflammatory environment that contributes the development and progression of most tumors. There is growing evidence that the mitochondrial ROS play a "central" role in inflammatory TME that ultimately exacerbates cancer [47,128]. Within the TME, active oncogenic signaling promotes cancer cells to autocrine and paracrine small molecular or cytokines to surrounding cells for tumor promotion.…”

“…On the other hand, high ROS inhibits T cell responses by suppressing the formation of TCR and MHC antigen complex, which promotes cancer progression through evading immune response [129]. Previously, the mechanisms of how oxidative stress modulates chronic inflammation-induced carcinogenesis from the TME point of view described in other reviews [5,47,130]. In this review, we mainly discuss the impact of mtROS stress on the TME, including cancer cells and various types of immune myeloid cells (Fig.…”

“…In conclusion, the production and regulation of ROS levels in the TMEassociated cancer and stromal cells play a decisive role in the progression of the disease. mtROS function is tightly controlled to maintain the balance through multiple mechanisms which are involved in inflammation and tumorigenesis [47]. However, extensive research is necessary to unveil the critical regulatory mechanisms driven by mtROS in tumor and tumor infiltrating immune cells for immune response in the TME.…”

The regulatory network of potential transcription factors and MiRNAs of mitochondria-related genes for sarcopenia

“…As the metabolic hub for energy production, mitochondria provide adenosine triphosphate (ATP) for skeletal muscle contraction through oxidative phosphorylation (OXPHOS). However, in the process of cellular senescence, there are numerous changes in mitochondria, such as decreased mitochondrial membrane potential, increased proton leakage, and reactive oxygen species production ( Amorim et al, 2022 ), which have been proven to have an important role in inflammatory responses ( Marchi et al, 2022 ), insulin resistance ( Hayden, 2022 ), as well as aging ( Miwa et al, 2022 ). Mitochondrial dysfunction could lead to the onset and progression of sarcopenia, a better understanding of the regulation factors controlling mitochondrial gene expression level and driving mitochondrial dysfunction in sarcopenia is therefore needed.…”