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Review
. 2023 Oct 12:14:1266461.
doi: 10.3389/fimmu.2023.1266461. eCollection 2023.

Mitochondrial antiviral signaling protein: a potential therapeutic target in renal disease

Meng Wu  1 , Zhiyin Pei  1 , Guangfeng Long  1 , Hongbing Chen  1 , Zhanjun Jia  2   3 , Weiwei Xia  1   2   3
Affiliations
Review

Mitochondrial antiviral signaling protein: a potential therapeutic target in renal disease

Meng Wu et al. Front Immunol. .

Abstract

Mitochondrial antiviral signaling protein (MAVS) is a key innate immune adaptor on the outer mitochondrial membrane that acts as a switch in the immune signal transduction response to viral infections. Some studies have reported that MAVS mediates NF-κB and type I interferon signaling during viral infection and is also required for optimal NLRP3 inflammasome activity. Recent studies have reported that MAVS is involved in various cancers, systemic lupus erythematosus, kidney diseases, and cardiovascular diseases. Herein, we summarize the structure, activation, pathophysiological roles, and MAVS-based therapies for renal diseases. This review provides novel insights into MAVS's role and therapeutic potential in the pathogenesis of renal diseases.

Keywords: MAVS; NLRP3; inflammation; innate immune; renal disease.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

Figures

Figure 1
Figure 1
Structures of MAVS. Schematic representation illustrating the three functional domains of MAVS: the CARD domain, proline-rich region, and TM.
Figure 2
Figure 2
Schematic representation of the antiviral signaling pathway model of MAVS. Viruses induce MAVS activation through TLR and RLR families. Homophilic interactions between CARD domains enable RIG-I and MDA5 to interact with MAVS. Upon TLR stimulation, MAVS triggers downstream signaling cascades by recruiting TRAF and TRIF. MAVS activates two cytosolic protein kinase complexes, leading to the production of immune factors. The TBK1 complex phosphorylates IRF-3/7, promoting the transcription of IFN genes. Simultaneously, the IKK complex activates NF-kB, resulting in the production of proinflammatory cytokines.
Figure 3
Figure 3
Overview of MAVS roles in renal diseases. (A) Multiple factors including hypoxia, IRI, sepsis, cisplatin, chronic kidney injury associated with proteinuria, UUO, hyperuricemia, aldosterone, and other risk factors activate MAVS and its downstream factor NLRP3 inflammasome. These activations stimulate processes such as inflammation, renal tubular epithelial cell injury, apoptosis, epithelial-mesenchymal transition, and tubulointerstitial fibrosis formation. (B) MAVS knockout contribute to the pathophysiology of diabetic nephropathy.
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Grants and funding

The authors declare financial support was received for the research, authorship, and/or publication of this article. This study was supported by a grant from the National Natural Science Foundation of China (no. 82070760, 82070701), grants from the Nanjing National Commission on Health and Family Planning (no. ZKX19042), grant from the Nanjing Medical Key Science and Technology Development Project Fund (No. YKK19105), and grants from Academic Technology Programof Nanjing Medical University (No. NMUB20210073).