The Role of Endoplasmic Reticulum Stress Response in Male Reproductive Physiology and Pathology: A Review

The World Journal of Men's Health
Keshab Kumar KarnaJong Kwan Park

Abstract

Endoplasmic reticulum (ER) stress, defined as prolonged disturbances in protein folding and accumulation of unfolded proteins in the ER. Perturbation of the ER, such as distribution of oxidative stress, iron imbalance, Ca2+ leakage, protein overload, and hypoxia, can cause ER stress. The cell reacts to ER stress by activating protective pathways, called the unfolded protein response (UPR), which is comprised of cellular mechanisms aimed for maintaining cellular homeostasis or, in case of excessively severe stress, at the initiation of cellular apoptosis. The three UPR signaling pathways from the ER stress sensors are initiated by activating transcription factor 6, inositol requiring enzyme 1, and protein kinase RNA-activated-like ER kinase. A number of physiological and pathological conditions, environmental toxicants and variety of pharmacological agents showed disruption of proper ER functions and thereby cause ER stress in male reproductive organ in rat model. The present review summarizes the existing data concerning the molecular and biological mechanism of ER stress in male reproduction and male infertility. ER stress initiated cell death pathway has been related to several diseases, including hypoxia, heath disease, diab...Continue Reading

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Citations

Nov 7, 2019·International Journal of Molecular Sciences·Joana SantiagoMargarida Fardilha
Dec 10, 2019·Molecular Human Reproduction·J SantiagoJ V Silva
Jan 8, 2021·Molecular Human Reproduction·Miyuki HaradaYutaka Osuga
Dec 24, 2020·Clinical Science·Beatriz Delgado-ValeroErnesto Martínez-Martínez
Feb 6, 2021·Molecular Human Reproduction·Miyuki HaradaYutaka Osuga
May 4, 2021·Frontiers in Cell and Developmental Biology·Shenae L CafeElizabeth G Bromfield
May 26, 2021·Epigenetics & Chromatin·Eli SellemLaurent Schibler

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Methods Mentioned

BETA
protein folding

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis