A review for the correlation between optic atrophy 1-dependent mitochondrial fusion and cardiovascular disorders

Yao, Bi-Feng; Luo, Xiu-Ju; Peng, Jun

doi:10.1016/j.ijbiomac.2023.127910

Cited by 1 publication

(1 citation statement)

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“…This pathway protects and repairs damaged mitochondria by transmitting signals of mitochondrial damage to the nucleus, which promotes the high expression of nuclear-encoded mitochondrial stress genes [8]. Mitochondrial fission and fusion ensure that damaged mitochondria are separated and removed in a timely manner and maintain the homeostasis of mitochondria and their contents [9]. Current studies have shown that mitochondria first initiate the fusion process to restore normal mitochondrial function; when mitochondrial fusion fails to maintain normal physiological function when the injury is further aggravated then mitochondrial fission is initiated to remove severely damaged mitochondria [10].…”

Section: Introductionmentioning

confidence: 99%

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: Introductionmentioning

confidence: 99%