FUN14 domain‐containing 1-mediated mitophagy suppresses interleukin-1β production in macrophages

Huang, Jia; Zhu, Tengfei; Rong, Rong; You, Mengling; Ji, Dan; Li, Haibo

doi:10.1016/j.intimp.2020.106964

Cited by 9 publications

(8 citation statements)

References 28 publications

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“…Impaired mitochondria with an altered calcium buffering system generate less ATP and more ROS, eventually leading to mitochondria-related cell apoptosis. Studies have established an association between FUNDC1 and ROS generation and apoptosis (Zhang et al, 2016;Wu et al, 2017;Wu et al, 2019b;Huang et al, 2020;Jiang et al, 2021). Huang et al found that ablation of FUNDC1 enhances the production of ROS and interleukin 1-β (IL1-β) in macrophages treated with combined lipopolysaccharide (LPS) and nigericin in vivo and in vitro through the regulation of mitophagy, while the overexpression of FUNDC1 (but not of its Y18A/L21A mutant) can reverse this effect in vitro (Huang et al, 2020).…”

Section: Fundc1 Regulates the Production Of Ros And Apoptosis In Cvdsmentioning

confidence: 99%

“…Studies have established an association between FUNDC1 and ROS generation and apoptosis (Zhang et al, 2016;Wu et al, 2017;Wu et al, 2019b;Huang et al, 2020;Jiang et al, 2021). Huang et al found that ablation of FUNDC1 enhances the production of ROS and interleukin 1-β (IL1-β) in macrophages treated with combined lipopolysaccharide (LPS) and nigericin in vivo and in vitro through the regulation of mitophagy, while the overexpression of FUNDC1 (but not of its Y18A/L21A mutant) can reverse this effect in vitro (Huang et al, 2020). In the H9C2 model of septic cardiomyopathy, Jiang et al found that the ROS generation and apoptosis related to FUNDC1mediated mitophagy can be attenuated and inhibited by irisin (Jiang et al, 2021).…”

Section: Fundc1 Regulates the Production Of Ros And Apoptosis In Cvdsmentioning

confidence: 99%

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FUNDC1: A Promising Mitophagy Regulator at the Mitochondria-Associated Membrane for Cardiovascular Diseases

Shao

et al. 2021

Front. Cell Dev. Biol.

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Mitochondrial autophagy (or mitophagy) regulates the mitochondrial network and function to contribute to multiple cellular processes. The protective effect of homeostatic mitophagy in cardiovascular diseases (CVDs) has attracted increasing attention. FUN14 domain containing 1 (FUNDC1), an identified mitophagy receptor, plays an essential role in CVDs. Different expression levels of FUNDC1 and its phosphorylated state at different sites alleviate or exacerbate hypoxia and ischemia/reperfusion injury, cardiac hypertrophy, or metabolic damage through promotion or inhibition of mitophagy. In addition, FUNDC1 can be enriched at contact sites between mitochondria and the endoplasmic reticulum (ER), determining the formation of mitochondria-associated membranes (MAMs) that regulate cellular calcium (Ca2+) homeostasis and mitochondrial dynamics to prevent heart dysfunction. Moreover, FUNDC1 has also been involved in inflammatory cardiac diseases such as septic cardiomyopathy. In this review, we collect and summarize the evidence on the roles of FUNDC1 exclusively in various CVDs, describing its interactions with different cellular organelles, its involvement in multiple cellular processes, and its associated signaling pathways. FUNDC1 may become a promising therapeutic target for the prevention and management of various CVDs.

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Section: Fundc1 Regulates the Production Of Ros And Apoptosis In Cvdsmentioning

confidence: 99%

Section: Fundc1 Regulates the Production Of Ros And Apoptosis In Cvdsmentioning

confidence: 99%

FUNDC1: A Promising Mitophagy Regulator at the Mitochondria-Associated Membrane for Cardiovascular Diseases

Shao

et al. 2021

Front. Cell Dev. Biol.

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“…They first demonstrated that FUNDC1 alleviated ICH-induced inflammation by inhibiting NLRP3-mediated inflammation by promoting mitophagy. In addition, the inhibition of FUNDC1-mediated mitophagy markedly increased IL-1β production in vitro and in vivo ( Huang et al, 2020 ). Optineurin is an autophagy receptor and an autophagy inducer that participates in the initiation of autophagosome membrane formation ( Ying and Yue, 2016 ; Qiu et al, 2022 ).…”

Section: Autophagy Regulates Inflammation In Ichmentioning

confidence: 99%

“…In addition, the inhibition of FUNDC1-mediated mitophagy markedly increased IL-1β production in vitro and in vivo (Huang et al, 2020). Optineurin is an autophagy receptor and an autophagy inducer that participates in the initiation of autophagosome membrane formation (Ying and Yue, 2016;Qiu et al, 2022) ICH brain flecked for iTRAQ-based quantitative proteomics (Cheng et al, 2021).…”

Section: Mitophagy Inhibits Nlrp3 Inflammasomementioning

confidence: 99%

Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?

Lenahan³

et al. 2023

Front. Cell. Neurosci.

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Intracerebral hemorrhage (ICH) is the second-largest stroke subtype and has a high mortality and disability rate. Secondary brain injury (SBI) is delayed after ICH. The main contributors to SBI are inflammation, oxidative stress, and excitotoxicity. Harmful substances from blood and hemolysis, such as hemoglobin, thrombin, and iron, induce SBI. When cells suffer stress, a critical protective mechanism called “autophagy” help to maintain the homeostasis of damaged cells, remove harmful substances or damaged organelles, and recycle them. Autophagy plays a critical role in the pathology of ICH, and its function remains controversial. Several lines of evidence demonstrate a pro-survival role for autophagy in ICH by facilitating the removal of damaged proteins and organelles. However, many studies have found that heme and iron can aggravate SBI by enhancing autophagy. Autophagy and inflammation are essential culprits in the progression of brain injury. It is a fascinating hypothesis that autophagy regulates inflammation in ICH-induced SBI. Autophagy could degrade and clear pro-IL-1β and apoptosis-associated speck-like protein containing a CARD (ASC) to antagonize NLRP3-mediated inflammation. In addition, mitophagy can remove endogenous activators of inflammasomes, such as reactive oxygen species (ROS), inflammatory components, and cytokines, in damaged mitochondria. However, many studies support the idea that autophagy activates microglia and aggravates microglial inflammation via the toll-like receptor 4 (TLR4) pathway. In addition, autophagy can promote ICH-induced SBI through inflammasome-dependent NLRP6-mediated inflammation. Moreover, some resident cells in the brain are involved in autophagy in regulating inflammation after ICH. Some compounds or therapeutic targets that regulate inflammation by autophagy may represent promising candidates for the treatment of ICH-induced SBI. In conclusion, the mutual regulation of autophagy and inflammation in ICH is worth exploring. The control of inflammation by autophagy will hopefully prove to be an essential treatment target for ICH.

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“…Our previous work has revealed that FUNDC1mediated mitophagy suppressed hepatocarcinogenesis by suppression of inflammasome activation by diethylnitrosamine (DEN) in liver (Li et al, 2019). Interestingly, two recently reports have also demonstrated that FUNDC1-mediated mitophagy suppresses LPS plus nigericin-mediated IL-1β production or apoptosis in the lung induced by LPS through inhibition of ROS-NLRP3, indicating that both FUNDC1-mediated mitophagy and its related inflammatory response are involved in SICM development (Huang et al, 2020;Pan et al, 2021).…”

Section: Fundc1 and Sepsis-induced Cardiomyopathymentioning

confidence: 99%

The Emerging Role of FUNDC1-Mediated Mitophagy in Cardiovascular Diseases

Liu

Chen

2021

Front. Physiol.

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Mitochondria are highly dynamic organelles and play essential role in ATP synthase, ROS production, innate immunity, and apoptosis. Mitochondria quality control is critical for maintaining the cellular function in response to cellular stress, growth, and differentiation Signals. Damaged or unwanted mitochondria are selectively removed by mitophagy, which is a crucial determinant of cell viability. Mitochondria-associated Endoplasmic Reticulum Membranes (MAMs) are the cellular structures that connect the ER and mitochondria and are involved in calcium signaling, lipid transfer, mitochondrial dynamic, and mitophagy. Abnormal mitochondrial quality induced by mitophagy impairment and MAMs dysfunction is associated with many diseases, including cardiovascular diseases (CVDs), metabolic syndrome, and neurodegenerative diseases. As a mitophagy receptor, FUNDC1 plays pivotal role in mitochondrial quality control through regulation of mitophagy and MAMs and is closely related to the occurrence of several types of CVDs. This review covers the regulation mechanism of FUNDC1-mediated mitophagy and MAMs formation, with a particular focus on its role in CVDs.

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FUN14 domain‐containing 1-mediated mitophagy suppresses interleukin-1β production in macrophages

Cited by 9 publications

References 28 publications

FUNDC1: A Promising Mitophagy Regulator at the Mitochondria-Associated Membrane for Cardiovascular Diseases

FUNDC1: A Promising Mitophagy Regulator at the Mitochondria-Associated Membrane for Cardiovascular Diseases

Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?

The Emerging Role of FUNDC1-Mediated Mitophagy in Cardiovascular Diseases

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