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Necroptosis in stressed ovary

Stress is deeply rooted in the modern society due to limited resources and large competition to achieve the desired goal. Women are more frequently exposed to several stressors during their reproductive age that trigger generation of reactive oxygen species (ROS). Accumulation of ROS in the body cau...

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Autores principales: Chaudhary, Govind R., Yadav, Pramod K., Yadav, Anil K., Tiwari, Meenakshi, Gupta, Anumegha, Sharma, Alka, Pandey, Ashutosh N., Pandey, Ajai K., Chaube, Shail K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6340166/
https://www.ncbi.nlm.nih.gov/pubmed/30665407
http://dx.doi.org/10.1186/s12929-019-0504-2
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author Chaudhary, Govind R.
Yadav, Pramod K.
Yadav, Anil K.
Tiwari, Meenakshi
Gupta, Anumegha
Sharma, Alka
Pandey, Ashutosh N.
Pandey, Ajai K.
Chaube, Shail K.
author_facet Chaudhary, Govind R.
Yadav, Pramod K.
Yadav, Anil K.
Tiwari, Meenakshi
Gupta, Anumegha
Sharma, Alka
Pandey, Ashutosh N.
Pandey, Ajai K.
Chaube, Shail K.
author_sort Chaudhary, Govind R.
collection PubMed
description Stress is deeply rooted in the modern society due to limited resources and large competition to achieve the desired goal. Women are more frequently exposed to several stressors during their reproductive age that trigger generation of reactive oxygen species (ROS). Accumulation of ROS in the body causes oxidative stress (OS) and adversely affects ovarian functions. The increased OS triggers various cell death pathways in the ovary. Beside apoptosis and autophagy, OS trigger necroptosis in granulosa cell as well as in follicular oocyte. The OS could activate receptor interacting protein kinase-1(RIPK1), receptor interacting protein kinase-3 (RIPK3) and mixed lineage kinase domain-like protein (MLKL) to trigger necroptosis in mammalian ovary. The granulosa cell necroptosis may deprive follicular oocyte from nutrients, growth factors and survival factors. Under these conditions, oocyte becomes more susceptible towards OS-mediated necroptosis in the follicular oocytes. Induction of necroptosis in encircling granulosa cell and oocyte may lead to follicular atresia. Indeed, follicular atresia is one of the major events responsible for the elimination of majority of germ cells from cohort of ovary. Thus, the inhibition of necroptosis could prevent precautious germ cell depletion from ovary that may cause reproductive senescence and early menopause in several mammalian species including human.
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spelling pubmed-63401662019-01-24 Necroptosis in stressed ovary Chaudhary, Govind R. Yadav, Pramod K. Yadav, Anil K. Tiwari, Meenakshi Gupta, Anumegha Sharma, Alka Pandey, Ashutosh N. Pandey, Ajai K. Chaube, Shail K. J Biomed Sci Review Stress is deeply rooted in the modern society due to limited resources and large competition to achieve the desired goal. Women are more frequently exposed to several stressors during their reproductive age that trigger generation of reactive oxygen species (ROS). Accumulation of ROS in the body causes oxidative stress (OS) and adversely affects ovarian functions. The increased OS triggers various cell death pathways in the ovary. Beside apoptosis and autophagy, OS trigger necroptosis in granulosa cell as well as in follicular oocyte. The OS could activate receptor interacting protein kinase-1(RIPK1), receptor interacting protein kinase-3 (RIPK3) and mixed lineage kinase domain-like protein (MLKL) to trigger necroptosis in mammalian ovary. The granulosa cell necroptosis may deprive follicular oocyte from nutrients, growth factors and survival factors. Under these conditions, oocyte becomes more susceptible towards OS-mediated necroptosis in the follicular oocytes. Induction of necroptosis in encircling granulosa cell and oocyte may lead to follicular atresia. Indeed, follicular atresia is one of the major events responsible for the elimination of majority of germ cells from cohort of ovary. Thus, the inhibition of necroptosis could prevent precautious germ cell depletion from ovary that may cause reproductive senescence and early menopause in several mammalian species including human. BioMed Central 2019-01-21 /pmc/articles/PMC6340166/ /pubmed/30665407 http://dx.doi.org/10.1186/s12929-019-0504-2 Text en © The Author(s). 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Chaudhary, Govind R.
Yadav, Pramod K.
Yadav, Anil K.
Tiwari, Meenakshi
Gupta, Anumegha
Sharma, Alka
Pandey, Ashutosh N.
Pandey, Ajai K.
Chaube, Shail K.
Necroptosis in stressed ovary
title Necroptosis in stressed ovary
title_full Necroptosis in stressed ovary
title_fullStr Necroptosis in stressed ovary
title_full_unstemmed Necroptosis in stressed ovary
title_short Necroptosis in stressed ovary
title_sort necroptosis in stressed ovary
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6340166/
https://www.ncbi.nlm.nih.gov/pubmed/30665407
http://dx.doi.org/10.1186/s12929-019-0504-2
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