Skeletal muscle redox signaling in rheumatoid arthritis

Steinz, Maarten M.; Santos‐Alves, Estela; Lanner, Johanna T.

doi:10.1042/cs20190728

Cited by 25 publications

(15 citation statements)

References 130 publications

(233 reference statements)

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“…Our data showed that after short period hypoxia induction, the expression level of HIF-1a in Claudin-5 112Δ5 and Claudin-5 297Δ4 mutant bEnd.3 cells was significantly lower than that in Claudin-5 wt bEnd.3 cells. As a downstream effecter of iNOS, ROS is usually produced by various sources in the CNS, including mitochondria, NADPH oxidase, and NOS ( Galley, 2011 ; Chan and Chan, 2014 ; Steinz et al, 2020 ). We used DCFH-DA to measure the ROS level in endothelial cells, and the data showed that the ROS generation in Claudin-5 wt bEnd.3 cells were higher than those in Claudin-5 112Δ5 and Claudin-5 297Δ4 bEnd.3 cells in response to early hypoxia stimulation.…”

Section: Discussionmentioning

confidence: 99%

Claudin-5 Affects Endothelial Autophagy in Response to Early Hypoxia

Zhong

et al. 2021

Front. Physiol.

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Hypoxic injury to cerebrovascular endothelial cells (ECs) after stroke leads to blood-brain barrier (BBB) dysfunction, which is commonly associated with disruptions of endothelial tight junctions (TJs) and increased permeability. Therefore, maintaining the structural integrity and proper function of the BBB is essential for the homeostasis and physiological function of the central nervous system (CNS). Our previous study revealed that autophagy functions on protecting the BBB by regulating the dynamics of Claudin-5, the essential TJ protein, under short-term starvation or hypoxia conditions. Here, we show that in zebrafish and in vitro cells, loss of membranous Claudin-5 conversely determine the occurrence of hypoxia-induced autophagy in cerebrovascular ECs. Absence of endothelial Claudin-5 could partly attenuate endothelial cell apoptosis caused by short-term hypoxic injury. Mechanism studies revealed that under hypoxic conditions, the existence of membranous Claudin-5 affects the stimulation of hypoxia inducible factor 1 subunit alpha (HIF-1a) and the inducible nitric oxide synthase (iNOS), which are responsible for the translocation of and endocytosis of caveole-packaged Claudin-5 into cytosol. Meanwhile, loss of Claudin-5 affects the generation of reactive oxygen species (ROS) and the downstream expression of BCL2/adenovirus E1B 19kDa protein interacting protein 3 (Bnip3). These together suppress the endothelial autophagy under hypoxia. This finding provides a theoretical basis for clarifying the mechanism of hypoxia-induced BBB injury and its potential protection mechanisms.

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Section: Discussionmentioning

confidence: 99%

Claudin-5 Affects Endothelial Autophagy in Response to Early Hypoxia

Zhong

et al. 2021

Front. Physiol.

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“…Skeletal muscle contains three NOS subtypes, which are neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial NOS (eNOS) ( Hussain et al, 1985 ; Ohkoshi et al, 1997 ; Tengan et al, 2012 ). NOS enzymes are also regards as a origin of O 2 •- production that occurs when NOS is uncoupled from its substrate L-Arg and its cofactor BH 4 ( Luo et al, 2014 ; Steinz et al, 2020 ). NO • is a radical because it contains one unpaired electron on the antibonding ( Valko et al, 2007 ).…”

Section: Reactive Oxygen/nitrogen Species and Antioxidants In Skeleta...mentioning

confidence: 99%

Mitochondrial Function and Reactive Oxygen/Nitrogen Species in Skeletal Muscle

Chen

Deng

et al. 2022

Front. Cell Dev. Biol.

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Skeletal muscle fibers contain a large number of mitochondria, which produce ATP through oxidative phosphorylation (OXPHOS) and provide energy for muscle contraction. In this process, mitochondria also produce several types of “reactive species” as side product, such as reactive oxygen species and reactive nitrogen species which have attracted interest. Mitochondria have been proven to have an essential role in the production of skeletal muscle reactive oxygen/nitrogen species (RONS). Traditionally, the elevation in RONS production is related to oxidative stress, leading to impaired skeletal muscle contractility and muscle atrophy. However, recent studies have shown that the optimal RONS level under the action of antioxidants is a critical physiological signal in skeletal muscle. Here, we will review the origin and physiological functions of RONS, mitochondrial structure and function, mitochondrial dynamics, and the coupling between RONS and mitochondrial oxidative stress. The crosstalk mechanism between mitochondrial function and RONS in skeletal muscle and its regulation of muscle stem cell fate and myogenesis will also be discussed. In all, this review aims to describe a comprehensive and systematic network for the interaction between skeletal muscle mitochondrial function and RONS.

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“…Systemic activation of pro-inflammatory molecules can potentially contribute to muscle fibre proteolysis and decrease protein synthesis [ 9 ]. Muscle injury has been regarded as an important contributor to RA-induced morbidity and mortality [ 13 ]. Bone and joint manifestations have a broad spectrum in COVID-19 with common viral arthralgia [ 14 ].…”

Section: Covid-19 and Ra Associationmentioning

confidence: 99%

COVID-19 and Rheumatoid Arthritis Crosstalk: Emerging Association, Therapeutic Options and Challenges

Dewanjee

Kandimalla

Kalra

et al. 2021

Cells

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Hyperactivation of immune responses resulting in excessive release of pro-inflammatory mediators in alveoli/lung structures is the principal pathological feature of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The cytokine hyperactivation in COVID-19 appears to be similar to those seen in rheumatoid arthritis (RA), an autoimmune disease. Emerging evidence conferred the severity and risk of COVID-19 to RA patients. Amid the evidence of musculoskeletal manifestations involving immune-inflammation-dependent mechanisms and cases of arthralgia and/or myalgia in COVID-19, crosstalk between COVID-19 and RA is often debated. The present article sheds light on the pathological crosstalk between COVID-19 and RA, the risk of RA patients in acquiring SARS-CoV-2 infection, and the aspects of SARS-CoV-2 infection in RA development. We also conferred whether RA can exacerbate COVID-19 outcomes based on available clinical readouts. The mechanistic overlapping in immune-inflammatory features in both COVID-19 and RA was discussed. We showed the emerging links of angiotensin-converting enzyme (ACE)-dependent and macrophage-mediated pathways in both diseases. Moreover, a detailed review of immediate challenges and key recommendations for anti-rheumatic drugs in the COVID-19 setting was presented for better clinical monitoring and management of RA patients. Taken together, the present article summarizes available knowledge on the emerging COVID-19 and RA crosstalk and their mechanistic overlaps, challenges, and therapeutic options.

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Skeletal muscle redox signaling in rheumatoid arthritis

Cited by 25 publications

References 130 publications

Claudin-5 Affects Endothelial Autophagy in Response to Early Hypoxia

Claudin-5 Affects Endothelial Autophagy in Response to Early Hypoxia

Mitochondrial Function and Reactive Oxygen/Nitrogen Species in Skeletal Muscle

COVID-19 and Rheumatoid Arthritis Crosstalk: Emerging Association, Therapeutic Options and Challenges

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