Fateme Zare

Dr. Fateme Zare

orcid

Research Focus & Metrics

Academic Career Length

12Years (2015-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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5 February 2020 in Journal of Cellular Physiology
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Journal Article
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FAFariba Akhondzadeh
Fariba Akhondzadeh
AAAkram Astani
Akram Astani
RNRazieh Najjari
Razieh Najjari
MSMorteza Samadi
Morteza Samadi
MRMohammad Ebrahim Rezvani
Mohammad Ebrahim Rezvani
FSFatemeh Safari
Fatemeh Safari

25 January 2021 in BioMed Research International
Verified
Journal Article
Open access
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HAHossein Ansariniya
Hossein Ansariniya
SSSeyed Mohammad Seifati
Seyed Mohammad Seifati
EZErfan Zaker
Erfan Zaker
FZFateme Zare
Fateme Zare
Severe Acute Respiratory Syndrome (SARS), Middle East Respiratory Syndrome (MERS), and Coronavirus Disease 2019 (COVID‐19) infections are the three epidemiological diseases caused by the Coronaviridae family. Perceiving the immune responses in these infections and the escape of viruses could help us design drugs and vaccines for confronting these infections. This review investigates the innate and adaptive immune responses reported in the infections of the three coronaviruses SARS, MERS, and COVID‐19. Moreover, the present study can trigger researchers to design and develop new vaccines and drugs based on immune system responses. In conclusion, due to the need for an effective and efficient immune stimulation against coronavirus, a combination of several strategies seems necessary for developing the vaccine.

20 December 2015 in Electronic Physiciane
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Journal Article
Open access
MOMaryam Okhovati
Maryam Okhovati
MZMorteza Zare
Morteza Zare
FZFateme Zare
Fateme Zare
MBMaliheh Sadat Bazrafshan
Maliheh Sadat Bazrafshan
ABAzam Bazrafshan
Azam Bazrafshan
Trends in Global Assisted Reproductive Technologies Research: a Scientometrics study

5 February 2020 in Journal of Biochemical and Molecular Toxicology
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MKMahdieh Kabiri
Mahdieh Kabiri
AHAnahid Hemmatpour
Anahid Hemmatpour
FZFateme Zare
Fateme Zare
HHHossein Hadinedoushan
Hossein Hadinedoushan
AKAlireza Karimollah
Alireza Karimollah

1 June 2021 in Clinical and Experimental Reproductive Medicine
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Journal Article
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KKKhadije Rezai Khanmohammad
Khadije Rezai Khanmohammad
MKMohammad Bagher Khalili
Mohammad Bagher Khalili
MSMaryam Sadeh
Maryam Sadeh
ATAli Reza Talebi
Ali Reza Talebi
AAAkram Astani
Akram Astani
FZFateme Zare
Fateme Zare
Objective: Uropathogenic Escherichia coli is known to cause urinary tract infections, and the endotoxin (lipopolysaccharide [LPS]) of this bacterium may cause deficiencies of sperm quality and morphology. In the present study, the effects of LPS on mouse sperm were studied, and the levels of interleukin (IL)-17A and possible changes in testis tissue were evaluated.Methods: LPS of uropathogenic E. coli was extracted using the methanol-chloroform method, followed confirmation using sodium dodecyl sulfate-polyacrylamide electrophoresis. Purified LPS (100 µg/kg) or phosphate-buffered saline was injected intraperitoneally into BALB/c mice for 7 days consecutively in the test and control groups, Mice were sacrificed on days 3, 7, and 42 after the first injection. Blood was tested for levels of IL-17A using the enzyme-linked immunosorbent assay method. Testis tissue and sperm were collected from each mouse and were studied according to standard protocols. Results: The mean sperm count and motility significantly decreased (p=0.03) at 3, 7, and 42 days after the injections. The level of IL-17A in the test groups increased, but not significantly (p=0.8, p=0.11, and p=0.15, respectively). Microscopic studies showed no obvious changes in the morphology of the testis tissue; however, significant changes were observed in the cellular parenchyma on day 42. Conclusion: LPS can stimulate the immune system to produce pro-inflammatory cytokines, resulting in an immune response in the testis and ultimately leading to deficiency in sperm parameters and testis tissue damage. In addition, the presence of LPS could significantly impair sperm parameters, as shown by the finding of decreased motility.

9 June 2025 in Frontiers in Cell and Developmental Biology
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MKMohammad Masoud Khodaei
Mohammad Masoud Khodaei
ZNZahra Noori
Zahra Noori
FZFateme Zare
Fateme Zare
AMAhmad Meshkin
Ahmad Meshkin
Ferroptosis is characterized as a specialized type of regulated cellular death that relies on iron and lipid peroxidation, which has recently been highlighted as playing a crucial role in the etiology of recurrent miscarriage (RM). Ferroptosis in RM is driven by dysregulated iron metabolism and increased oxidative stress, resulting from impaired antioxidant defense, which leads to lipid peroxidation and consequent cell death in trophoblasts. The cellular changes compromise placental development and impair trophoblast invasion and maternal-fetal tolerance. Therapeutic interventions targeting ferroptosis are promising for the mitigation of its effects and improvement of pregnancy outcomes. Strategies include Glutathione Peroxidase 4 (GPX4) activity enhancement, glutathione replenishment, ferroptosis inhibitors, and iron metabolism modulation. Further, new strategies targeting non-coding RNAs, and epigenetic regulators emphasize ferroptosis as a viable therapeutic target. This review emphasizes the importance of ferroptosis in the pathophysiology of RM and highlights its potential for guiding innovative treatments.