Glial Activation, Mitochondrial Imbalance, and Akt/mTOR Signaling May Be Potential Mechanisms of Cognitive Impairment in Heart Failure Mice

Wu, Yanan; Zhou, Kaiyi; Liu, Baiyang; Xu, Jindong; Lei, Liming; Hu, Jiaqi; Cheng, Xiao; Zhong, Feng; Wang, Sheng

doi:10.1007/s12640-023-00655-2

Cited by 1 publication

(1 citation statement)

References 76 publications

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“…It was shown above that HtrA2/Omi deficiency leads to abnormal mitochondrial dynamics by promoting mitochondrial division. In the hippocampus of heart failure mice, mitochondrial fission gene DRP1 has been reported to be increased, and damaged mitochondria release excess ROS and have a reduced ability to produce ATP [93]. Furthermore, reduced mitochondrial mass and activity was found after overexpression of mitochondrial fission factor in the breast cancer cell line MCF7, and analysis of metabolic fluxes using Seahorse XFe96 revealed reduced levels of oxidative phosphorylation and glycolysis in this cell [94].…”

Section: Oxphos Complex Abnormalities Promote Pro-inflammatory Macrop...mentioning

confidence: 98%

HTRA2/OMI-Mediated Mitochondrial Quality Control Alters Macrophage Polarization Affecting Systemic Chronic Inflammation

Liu,

Yan,

Yuan

et al. 2024

IJMS

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Systemic chronic inflammation (SCI) due to intrinsic immune over-activation is an important factor in the development of many noninfectious chronic diseases, such as neurodegenerative diseases and diabetes mellitus. Among these immune responses, macrophages are extensively involved in the regulation of inflammatory responses by virtue of their polarization plasticity; thus, dysregulation of macrophage polarization direction is one of the potential causes of the generation and maintenance of SCI. High-temperature demand protein A2 (HtrA2/Omi) is an important regulator of mitochondrial quality control, not only participating in the degradation of mis-accumulated proteins in the mitochondrial unfolded protein response (UPRmt) to maintain normal mitochondrial function through its enzymatic activity, but also participating in the regulation of mitochondrial dynamics-related protein interactions to maintain mitochondrial morphology. Recent studies have also reported the involvement of HtrA2/Omi as a novel inflammatory mediator in the regulation of the inflammatory response. HtrA2/Omi regulates the inflammatory response in BMDM by controlling TRAF2 stabilization in a collagen-induced arthritis mouse model; the lack of HtrA2 ameliorates pro-inflammatory cytokine expression in macrophages. In this review, we summarize the mechanisms by which HtrA2/Omi proteins are involved in macrophage polarization remodeling by influencing macrophage energy metabolism reprogramming through the regulation of inflammatory signaling pathways and mitochondrial quality control, elucidating the roles played by HtrA2/Omi proteins in inflammatory responses. In conclusion, interfering with HtrA2/Omi may become an important entry point for regulating macrophage polarization, providing new research space for developing HtrA2/Omi-based therapies for SCI.

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Section: Oxphos Complex Abnormalities Promote Pro-inflammatory Macrop...mentioning

confidence: 98%

HTRA2/OMI-Mediated Mitochondrial Quality Control Alters Macrophage Polarization Affecting Systemic Chronic Inflammation

Liu,

Yan,

Yuan

et al. 2024

IJMS

View full text Add to dashboard Cite

show abstract

Glial Activation, Mitochondrial Imbalance, and Akt/mTOR Signaling May Be Potential Mechanisms of Cognitive Impairment in Heart Failure Mice

Cited by 1 publication

References 76 publications

HTRA2/OMI-Mediated Mitochondrial Quality Control Alters Macrophage Polarization Affecting Systemic Chronic Inflammation

HTRA2/OMI-Mediated Mitochondrial Quality Control Alters Macrophage Polarization Affecting Systemic Chronic Inflammation

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