Protective Role of MAVS Signaling for Murine Lipopolysaccharide-Induced Acute Kidney Injury
Despite treatment advances, acute kidney injury (AKI)-related mortality rates are still high in hospitalized adults, often due to sepsis. Sepsis and AKI could synergistically worsen the outcomes of critically ill patients. TLR4 signaling and mitochondrial antiviral signaling protein (MAVS) signaling...
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Published in | ImmunoHorizons Vol. 8; no. 1; pp. 1 - 18 |
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Main Authors | , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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01.01.2024
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Abstract | Despite treatment advances, acute kidney injury (AKI)-related mortality rates are still high in hospitalized adults, often due to sepsis. Sepsis and AKI could synergistically worsen the outcomes of critically ill patients. TLR4 signaling and mitochondrial antiviral signaling protein (MAVS) signaling are innate immune responses essential in kidney diseases, but their involvement in sepsis-associated AKI (SA-AKI) remains unclear. We studied the role of MAVS in kidney injury related to the TLR4 signaling pathway using a murine LPS-induced AKI model in wild-type and MAVS-knockout mice. We confirmed the importance of M1 macrophage in SA-AKI through in vivo assessment of inflammatory responses. The TLR4 signaling pathway was upregulated in activated bone marrow-derived macrophages, in which MAVS helped maintain the LPS-suppressed TLR4 mRNA level. MAVS regulated redox homeostasis via NADPH oxidase Nox2 and mitochondrial reverse electron transport in macrophages to alleviate the TLR4 signaling response to LPS. Hypoxia-inducible factor 1α (HIF-1α) and AP-1 were key regulators of TLR4 transcription and connected MAVS-dependent reactive oxygen species signaling with the TLR4 pathway. Inhibition of succinate dehydrogenase could partly reduce inflammation in LPS-treated bone marrow-derived macrophages without MAVS. These findings highlight the renoprotective role of MAVS in LPS-induced AKI by regulating reactive oxygen species generation-related genes and maintaining redox balance. Controlling redox homeostasis through MAVS signaling may be a promising therapy for SA-AKI. |
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AbstractList | Despite treatment advances, acute kidney injury (AKI)-related mortality rates are still high in hospitalized adults, often due to sepsis. Sepsis and AKI could synergistically worsen the outcomes of critically ill patients. TLR4 signaling and mitochondrial antiviral signaling protein (MAVS) signaling are innate immune responses essential in kidney diseases, but their involvement in sepsis-associated AKI (SA-AKI) remains unclear. We studied the role of MAVS in kidney injury related to the TLR4 signaling pathway using a murine LPS-induced AKI model in wild-type and MAVS-knockout mice. We confirmed the importance of M1 macrophage in SA-AKI through in vivo assessment of inflammatory responses. The TLR4 signaling pathway was upregulated in activated bone marrow-derived macrophages, in which MAVS helped maintain the LPS-suppressed TLR4 mRNA level. MAVS regulated redox homeostasis via NADPH oxidase Nox2 and mitochondrial reverse electron transport in macrophages to alleviate the TLR4 signaling response to LPS. Hypoxia-inducible factor 1α (HIF-1α) and AP-1 were key regulators of TLR4 transcription and connected MAVS-dependent reactive oxygen species signaling with the TLR4 pathway. Inhibition of succinate dehydrogenase could partly reduce inflammation in LPS-treated bone marrow-derived macrophages without MAVS. These findings highlight the renoprotective role of MAVS in LPS-induced AKI by regulating reactive oxygen species generation-related genes and maintaining redox balance. Controlling redox homeostasis through MAVS signaling may be a promising therapy for SA-AKI. Despite treatment advances, acute kidney injury (AKI)-related mortality rates are still high in hospitalized adults, often due to sepsis. Sepsis and AKI could synergistically worsen the outcomes of critically ill patients. TLR4 signaling and mitochondrial antiviral signaling protein (MAVS) signaling are innate immune responses essential in kidney diseases, but their involvement in sepsis-associated AKI (SA-AKI) remains unclear. We studied the role of MAVS in kidney injury related to the TLR4 signaling pathway using a murine LPS-induced AKI model in wild-type and MAVS-knockout mice. We confirmed the importance of M1 macrophage in SA-AKI through in vivo assessment of inflammatory responses. The TLR4 signaling pathway was upregulated in activated bone marrow-derived macrophages, in which MAVS helped maintain the LPS-suppressed TLR4 mRNA level. MAVS regulated redox homeostasis via NADPH oxidase Nox2 and mitochondrial reverse electron transport in macrophages to alleviate the TLR4 signaling response to LPS. Hypoxia-inducible factor 1α (HIF-1α) and AP-1 were key regulators of TLR4 transcription and connected MAVS-dependent reactive oxygen species signaling with the TLR4 pathway. Inhibition of succinate dehydrogenase could partly reduce inflammation in LPS-treated bone marrow-derived macrophages without MAVS. These findings highlight the renoprotective role of MAVS in LPS-induced AKI by regulating reactive oxygen species generation-related genes and maintaining redox balance. Controlling redox homeostasis through MAVS signaling may be a promising therapy for SA-AKI. Abstract Despite treatment advances, acute kidney injury (AKI)–related mortality rates are still high in hospitalized adults, often due to sepsis. Sepsis and AKI could synergistically worsen the outcomes of critically ill patients. TLR4 signaling and mitochondrial antiviral signaling protein (MAVS) signaling are innate immune responses essential in kidney diseases, but their involvement in sepsis-associated AKI (SA-AKI) remains unclear. We studied the role of MAVS in kidney injury related to the TLR4 signaling pathway using a murine LPS-induced AKI model in wild-type and MAVS-knockout mice. We confirmed the importance of M1 macrophage in SA-AKI through in vivo assessment of inflammatory responses. The TLR4 signaling pathway was upregulated in activated bone marrow–derived macrophages, in which MAVS helped maintain the LPS-suppressed TLR4 mRNA level. MAVS regulated redox homeostasis via NADPH oxidase Nox2 and mitochondrial reverse electron transport in macrophages to alleviate the TLR4 signaling response to LPS. Hypoxia-inducible factor 1α (HIF-1α) and AP-1 were key regulators of TLR4 transcription and connected MAVS-dependent reactive oxygen species signaling with the TLR4 pathway. Inhibition of succinate dehydrogenase could partly reduce inflammation in LPS-treated bone marrow–derived macrophages without MAVS. These findings highlight the renoprotective role of MAVS in LPS-induced AKI by regulating reactive oxygen species generation-related genes and maintaining redox balance. Controlling redox homeostasis through MAVS signaling may be a promising therapy for SA-AKI. |
Author | Yuasa, Takahiro Kajikawa, Sho Tran, Trang Anh Thi Hayashi, Daiki Hoang, Linh Thuy Horikoshi, Keisuke Sako, Keisuke Yamamura, Yuta Shimizu, Miho Yoneda-Nakagawa, Shiori Oshima, Megumi Minami, Taichiro Wada, Takashi Toyama, Tadashi Iwata, Yasunori Kitajima, Shinji Sakai, Norihiko Yamazaki, Hiroka Hara, Akinori |
Author_xml | – sequence: 1 givenname: Trang Anh Thi orcidid: 0000-0002-8524-9571 surname: Tran fullname: Tran, Trang Anh Thi organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 2 givenname: Yasunori surname: Iwata fullname: Iwata, Yasunori organization: Division of Infection Control, Kanazawa University Hospital, Kanazawa, Japan – sequence: 3 givenname: Linh Thuy surname: Hoang fullname: Hoang, Linh Thuy organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 4 givenname: Shinji surname: Kitajima fullname: Kitajima, Shinji organization: Division of Blood Purification, Kanazawa University Hospital, Kanazawa, Japan – sequence: 5 givenname: Shiori surname: Yoneda-Nakagawa fullname: Yoneda-Nakagawa, Shiori organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 6 givenname: Megumi orcidid: 0000-0002-4108-5229 surname: Oshima fullname: Oshima, Megumi organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 7 givenname: Norihiko surname: Sakai fullname: Sakai, Norihiko organization: Division of Blood Purification, Kanazawa University Hospital, Kanazawa, Japan – sequence: 8 givenname: Tadashi orcidid: 0000-0003-0162-6286 surname: Toyama fullname: Toyama, Tadashi organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 9 givenname: Yuta orcidid: 0000-0003-3713-0733 surname: Yamamura fullname: Yamamura, Yuta organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 10 givenname: Hiroka surname: Yamazaki fullname: Yamazaki, Hiroka organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 11 givenname: Akinori surname: Hara fullname: Hara, Akinori organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 12 givenname: Miho surname: Shimizu fullname: Shimizu, Miho organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 13 givenname: Keisuke surname: Sako fullname: Sako, Keisuke organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 14 givenname: Taichiro orcidid: 0000-0002-2766-2528 surname: Minami fullname: Minami, Taichiro organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 15 givenname: Takahiro orcidid: 0009-0004-3556-935X surname: Yuasa fullname: Yuasa, Takahiro organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 16 givenname: Keisuke surname: Horikoshi fullname: Horikoshi, Keisuke organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 17 givenname: Daiki surname: Hayashi fullname: Hayashi, Daiki organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 18 givenname: Sho surname: Kajikawa fullname: Kajikawa, Sho organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan – sequence: 19 givenname: Takashi surname: Wada fullname: Wada, Takashi organization: Department of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan |
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Snippet | Despite treatment advances, acute kidney injury (AKI)-related mortality rates are still high in hospitalized adults, often due to sepsis. Sepsis and AKI could... Abstract Despite treatment advances, acute kidney injury (AKI)–related mortality rates are still high in hospitalized adults, often due to sepsis. Sepsis and... |
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SubjectTerms | Acute Kidney Injury - chemically induced Acute Kidney Injury - metabolism Animals Humans Lipopolysaccharides Mice Reactive Oxygen Species - metabolism Sepsis - metabolism Toll-Like Receptor 4 - metabolism |
Title | Protective Role of MAVS Signaling for Murine Lipopolysaccharide-Induced Acute Kidney Injury |
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