scholarly journals Role of ROS/RNS in Preeclampsia: Are Connexins the Missing Piece?

2020 ◽  
Vol 21 (13) ◽  
pp. 4698 ◽  
Author(s):  
María F. Rozas-Villanueva ◽  
Paola Casanello ◽  
Mauricio A. Retamal

Preeclampsia is a pregnancy complication that appears after 20 weeks of gestation and is characterized by hypertension and proteinuria, affecting both mother and offspring. The cellular and molecular mechanisms that cause the development of preeclampsia are poorly understood. An important feature of preeclampsia is an increase in oxygen and nitrogen derived free radicals (reactive oxygen species/reactive nitrogen species (ROS/RNS), which seem to be central players setting the development and progression of preeclampsia. Cell-to-cell communication may be disrupted as well. Connexins (Cxs), a family of transmembrane proteins that form hemichannels and gap junction channels (GJCs), are essential in paracrine and autocrine cell communication, allowing the movement of signaling molecules between cells as well as between the cytoplasm and the extracellular media. GJCs and hemichannels are fundamental for communication between endothelial and smooth muscle cells and, therefore, in the control of vascular contraction and relaxation. In systemic vasculature, the activity of GJCs and hemichannels is modulated by ROS and RNS. Cxs participate in the development of the placenta and are expressed in placental vasculature. However, it is unknown whether Cxs are modulated by ROS/RNS in the placenta, or whether this potential modulation contributes to the pathogenesis of preeclampsia. Our review addresses the possible role of Cxs in preeclampsia, and the plausible modulation of Cxs-formed channels by ROS and RNS. We suggest these factors may contribute to the development of preeclampsia.

Author(s):  
Kunli Zhang ◽  
Qiuyan Huang ◽  
Shoulong Deng ◽  
Yecheng Yang ◽  
Jianhao Li ◽  
...  

Pathogenic infections have badly affected public health and the development of the breeding industry. Billions of dollars are spent every year fighting against these pathogens. The immune cells of a host produce reactive oxygen species and reactive nitrogen species which promote the clearance of these microbes. In addition, autophagy, which is considered an effective method to promote the destruction of pathogens, is involved in pathological processes. As research continues, the interplay between autophagy and nitroxidative stress has become apparent. Autophagy is always intertwined with nitroxidative stress. Autophagy regulates nitroxidative stress to maintain homeostasis within an appropriate range. Intracellular oxidation, in turn, is a strong inducer of autophagy. Toll-like receptor 4 (TLR4) is a pattern recognition receptor mainly involved in the regulation of inflammation during infectious diseases. Several studies have suggested that TLR4 is also a key regulator of autophagy and nitroxidative stress. In this review, we describe the role of TLR4 in autophagy and oxidation, and focus on its function in influencing autophagy-nitroxidative stress interactions.


2004 ◽  
Vol 287 (2) ◽  
pp. C246-C256 ◽  
Author(s):  
Henry Jay Forman ◽  
Jon M. Fukuto ◽  
Martine Torres

Except for the role of NO in the activation of guanylate cyclase, which is well established, the involvement of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in signal transduction remains controversial, despite a large body of evidence suggestive of their participation in a variety of signaling pathways. Several problems have limited their acceptance as signaling molecules, with the major one being the difficulty in identifying the specific targets for each pathway and the chemical reactions supporting reversible oxidation of these signaling components, consistent with a second messenger role for ROS and RNS. Nevertheless, it has become clear that cysteine residues in the thiolate (i.e., ionized) form that are found in some proteins can be specific targets for reaction with H2O2 and RNS. This review focuses on the chemistry of the reversible oxidation of those thiolates, with a particular emphasis on the critical thiolate found in protein tyrosine phosphatases as an example.


2020 ◽  
Vol 21 (17) ◽  
pp. 6206 ◽  
Author(s):  
Joanna Pleńkowska ◽  
Magdalena Gabig-Cimińska ◽  
Paweł Mozolewski

This review discusses how oxidative stress (OS), an imbalance between oxidants and antioxidants in favor of the oxidants, increased production of reactive oxygen species (ROS)/reactive nitrogen species (RNS), and decreased concentration/activity of antioxidants affect the pathogenesis or cause the enhancement of psoriasis (Ps). Here, we also consider how ROS/RNS-induced stress modulates the activity of transcriptional factors and regulates numerous protein kinase cascades that participate in the regulation of crosstalk between autophagy, apoptosis, and regeneration. Answers to these questions will likely uncover novel strategies for the treatment of Ps. Action in the field will avoid destructive effects of ROS/RNS-mediated OS resulting in cellular dysfunction and cell death. The combination of the fragmentary information on the role of OS can provide evidence to extend the full picture of Ps.


2021 ◽  
Vol 28 ◽  
Author(s):  
Francisca Rivas ◽  
Carlos Poblete-Aro ◽  
María Elsa Pando ◽  
María José Allel ◽  
Valentina Fernandez ◽  
...  

: Aging is defined as the functional loss of tissues and organs over time. This is a biological, irreversible, progressive, and universal process that results from genetic and environmental factors, such as diet, physical activity, smoking, harmful alcohol consumption, and exposure to toxins, among others. Aging is a consequence of molecular and cellular damage built up over time. This damage begins with a gradual decrease in physical and mental capacity, thus increasing the risk of neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease. Neuronal, functional, and structural damage can be explained by an imbalance among free radicals, reactive oxygen species, reactive nitrogen species, and antioxidants, which finally lead to oxidative stress. Due to the key role of free radicals, reactive oxygen species, and reactive nitrogen species, antioxidant therapy may reduce the oxidative damage associated with neurodegeneration. Exogenous antioxidants are molecules that may help maintain the balance between the formation and elimination of free radicals, thus protecting the cell from their toxicity. Among them, polyphenols are a broad group of secondary plant metabolites with potent antioxidant properties. Here, we review several studies that show the potential role of polyphenol consumption to prevent, or slow down, harmful oxidative processes linked to neurodegenerative disorders.


Nanoscale ◽  
2021 ◽  
Author(s):  
Rachael Knoblauch ◽  
Chris Geddes

While the utility of reactive oxygen species in photodynamic therapies for both cancer treatments and antimicrobial applications has received much attention, the inherent potential of reactive nitrogen species (RNS) including...


2021 ◽  
Author(s):  
Cristina Parisi ◽  
Mariacristina Failla ◽  
Aurore Fraix ◽  
Luca Menilli ◽  
Francesca Moret ◽  
...  

The generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) as “unconventional” therapeutics with precise spatiotemporal control by using light stimuli may open entirely new horizons for innovative...


Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 466
Author(s):  
Rachid Skouta

Maintaining the physiological level of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in the body is highly important in the fight against radical species in the context of human health [...]


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