scholarly journals Reactive Oxygen Species, Apoptosis, and Mitochondrial Dysfunction in Hearing Loss

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Teru Kamogashira ◽  
Chisato Fujimoto ◽  
Tatsuya Yamasoba
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Hearing Loss ◽  
Reactive Oxygen ◽  
Necrotic Cell Death ◽  
Ros Production ◽  
Oxygen Species ◽  
Necrotic Cell ◽  
Cell Death Pathways ◽  
Age Related

Reactive oxygen species (ROS) production is involved in several apoptotic and necrotic cell death pathways in auditory tissues. These pathways are the major causes of most types of sensorineural hearing loss, including age-related hearing loss, hereditary hearing loss, ototoxic drug-induced hearing loss, and noise-induced hearing loss. ROS production can be triggered by dysfunctional mitochondrial oxidative phosphorylation and increases or decreases in ROS-related enzymes. Although apoptotic cell death pathways are mostly activated by ROS production, there are other pathways involved in hearing loss that do not depend on ROS production. Further studies of other pathways, such as endoplasmic reticulum stress and necrotic cell death, are required.

scholarly journals Mycobacterium tuberculosis Exploits Focal Adhesion Kinase to Induce Necrotic Cell Death and Inhibit Reactive Oxygen Species Production

2021 ◽  
Vol 12 ◽  
Author(s):  
Afrakoma Afriyie-Asante ◽  
Ankita Dabla ◽  
Amy Dagenais ◽  
Stefania Berton ◽  
Robin Smyth ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Mycobacterium Tuberculosis ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Reactive Oxygen ◽  
Necrotic Cell Death ◽  
Ros Production ◽  
Oxygen Species ◽  
Necrotic Cell

Tuberculosis is a deadly, contagious respiratory disease that is caused by the pathogenic bacterium Mycobacterium tuberculosis (Mtb). Mtb is adept at manipulating and evading host immunity by hijacking alveolar macrophages, the first line of defense against inhaled pathogens, by regulating the mode and timing of host cell death. It is established that Mtb infection actively blocks apoptosis and instead induces necrotic-like modes of cell death to promote disease progression. This survival strategy shields the bacteria from destruction by the immune system and antibiotics while allowing for the spread of bacteria at opportunistic times. As such, it is critical to understand how Mtb interacts with host macrophages to manipulate the mode of cell death. Herein, we demonstrate that Mtb infection triggers a time-dependent reduction in the expression of focal adhesion kinase (FAK) in human macrophages. Using pharmacological perturbations, we show that inhibition of FAK (FAKi) triggers an increase in a necrotic form of cell death during Mtb infection. In contrast, genetic overexpression of FAK (FAK+) completely blocked macrophage cell death during Mtb infection. Using specific inhibitors of necrotic cell death, we show that FAK-mediated cell death during Mtb infection occurs in a RIPK1-depedent, and to a lesser extent, RIPK3-MLKL-dependent mechanism. Consistent with these findings, FAKi results in uncontrolled replication of Mtb, whereas FAK+ reduces the intracellular survival of Mtb in macrophages. In addition, we demonstrate that enhanced control of intracellular Mtb replication by FAK+ macrophages is a result of increased production of antibacterial reactive oxygen species (ROS) as inhibitors of ROS production restored Mtb burden in FAK+ macrophages to same levels as in wild-type cells. Collectively, our data establishes FAK as an important host protective response during Mtb infection to block necrotic cell death and induce ROS production, which are required to restrict the survival of Mtb.

TNFα and reactive oxygen species in necrotic cell death

Cell Research ◽  
2008 ◽  
Vol 18 (3) ◽  
pp. 343-349 ◽  
Author(s):  
Michael J Morgan ◽  
You-Sun Kim ◽  
Zheng-gang Liu
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reactive Oxygen ◽  
Necrotic Cell Death ◽  
Oxygen Species ◽  
Necrotic Cell

scholarly journals HYD1-induced increase in reactive oxygen species leads to autophagy and necrotic cell death in multiple myeloma cells

2009 ◽  
Vol 8 (8) ◽  
pp. 2441-2451 ◽  
Author(s):  
Rajesh R. Nair ◽  
Michael F. Emmons ◽  
Anne E. Cress ◽  
Raul F. Argilagos ◽  
Kit Lam ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Multiple Myeloma ◽  
Cell Death ◽  
Reactive Oxygen ◽  
Necrotic Cell Death ◽  
Oxygen Species ◽  
Necrotic Cell ◽  
Myeloma Cells

Regulation of Fas (CD95)-induced apoptotic and necrotic cell death by reactive oxygen species in macrophages

2005 ◽  
Vol 203 (1) ◽  
pp. 78-84 ◽  
Author(s):  
Djordje Medan ◽  
Liying Wang ◽  
David Toledo ◽  
Bin Lu ◽  
Christian Stehlik ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reactive Oxygen ◽  
Necrotic Cell Death ◽  
Oxygen Species ◽  
Necrotic Cell

scholarly journals OTUD1 deubiquitylase regulates NF-κB- and KEAP1-mediated inflammatory responses and reactive oxygen species-associated cell death pathways

2021 ◽  
Author(s):  
Daisuke Oikawa ◽  
Min Gi ◽  
Hidetaka Kosako ◽  
Kouhei Shimizu ◽  
Hirotaka Takahashi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Stress Responses ◽  
Inflammatory Responses ◽  
Reactive Oxygen ◽  
Antioxidant Response ◽  
Oxygen Species ◽  
Ubiquitin Chain ◽  
Intrinsically Disordered ◽  
Cell Death Pathways

Deubiquitylating enzymes (DUBs) regulate numerous cellular functions by removing ubiquitin modifications. We examined the effects of 88 human DUBs on linear ubiquitin chain assembly complex (LUBAC)-induced NF-κB activation, and identified OTUD1 as a potent suppressor. OTUD1 regulates the canonical NF-κB pathway by hydrolysing K63-linked ubiquitin chains from NF-κB signalling factors, including LUBAC. OTUD1 negatively regulates the canonical NF-κB activation, apoptosis, and necroptosis, whereas OTUD1 upregulates the interferon (IFN) antiviral pathway. The N-terminal intrinsically disordered region of OTUD1, which contains an EGTE motif, is indispensable for KEAP1-binding and NF-κB suppression. OTUD1 is involved in the KEAP1-mediated antioxidant response and reactive oxygen species (ROS)-induced cell death, oxeiptosis. In Otud1-/--mice, inflammation, oxidative damage, and cell death were enhanced in inflammatory bowel disease, acute hepatitis, and sepsis models. Thus, OTUD1 is a crucial regulator for the inflammatory, innate immune, and oxidative stress responses and ROS-associated cell death pathways.

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