Zeina Harhous

ORCID: 0000-0001-7611-5160
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About
Contact & Profiles
Research Areas
  • Cardiac Ischemia and Reperfusion
  • Mitochondrial Function and Pathology
  • Cytokine Signaling Pathways and Interactions
  • Viral Infections and Immunology Research
  • MicroRNA in disease regulation
  • Cardiac Fibrosis and Remodeling
  • Adipose Tissue and Metabolism
  • Macrophage Migration Inhibitory Factor
  • Transplantation: Methods and Outcomes
  • Cancer, Hypoxia, and Metabolism
  • Anesthesia and Neurotoxicity Research
  • RNA Research and Splicing
  • Molecular Biology Techniques and Applications
  • Signaling Pathways in Disease
  • ATP Synthase and ATPases Research
  • COVID-19 Clinical Research Studies
  • Muscle Physiology and Disorders
  • COVID-19 Impact on Reproduction
  • Biochemical Analysis and Sensing Techniques
  • Metabolomics and Mass Spectrometry Studies
  • Genetic Neurodegenerative Diseases
  • Cancer-related molecular mechanisms research
  • Biomarkers in Disease Mechanisms
  • Phagocytosis and Immune Regulation
  • Carcinogens and Genotoxicity Assessment

Inserm
2019-2024

Laboratoire CarMeN
2018-2024

Université Claude Bernard Lyon 1
2018-2024

Lebanese American University
2020-2022

Harvard University
2022

Boston University
2022

Hospices Civils de Lyon
2019-2021

Institut National des Sciences Appliquées de Lyon
2019-2021

Lebanese University
2018-2019

Centre Hospitalier Vétérinaire Frégis
2019

Using a translational approach with an ST-segment myocardial infarction (STEMI) cohort and mouse model of infarction, we highlighted the role secreted IL-6 MCP-1 cytokines STAT3 pathway in heart macrophage recruitment activation. Cardiac myocytes secrete response to hypoxic stress, leading and/or polarization anti-inflammatory macrophages via pathway. In our preclinical neutralization or reduced infarct size. Together, data demonstrate that can be deleterious acute phase STEMI.

10.1016/j.jacbts.2024.01.019 article EN cc-by-nc-nd JACC Basic to Translational Science 2024-04-24

Following a prolonged exposure to hypoxia–reoxygenation, partial disruption of the ER-mitochondria tethering by mitofusin 2 (MFN2) knock-down decreases Ca2+ transfer between two organelles limits mitochondrial overload and prevents Ca2+-dependent opening permeability transition pore, i.e., cardiomyocyte cell death. The impact metabolic changes resulting from alteration this Ca2+crosstalk on tolerance hypoxia–reoxygenation injury remains fragmented different field expertise. >In study, we...

10.3390/cells9122542 article EN cc-by Cells 2020-11-25

During myocardial infarction, dysregulation of Ca2+ homeostasis between the reticulum, mitochondria, and cytosol occurs in cardiomyocytes leads to cell death. leak channels are thought be key regulators reticular survival. The present study aimed determine whether a particular channel, translocon, also known as translocation could relevant target against ischemia/reperfusion-mediated heart injury. To achieve this objective, we first used an intramyocardial adenoviral strategy express...

10.3390/cells9051319 article EN cc-by Cells 2020-05-25

Mitochondrial diseases are genetic disorders that lead to impaired mitochondrial function, resulting in exercise intolerance and muscle weakness. In patients, fatigue due defects oxidative capacities commonly precedes mice, deletion of the fast-twitch skeletal muscle-specific Tfam gene (Tfam KO) leads a deficit respiratory chain activity, severe weakness early death. Here, we performed time-course study muscular dysfunctions 11- 14-week-old KO i.e. before when mice about enter terminal...

10.1242/dmm.048981 article EN cc-by Disease Models & Mechanisms 2021-08-11

Gasoline exposure has been widely reported in the literature as being toxic to human health. However, exact underlying molecular mechanisms triggered by its inhalation have not thoroughly investigated. We herein present a model of sub-chronic, static gasoline vapor adult female C57BL/6 mice. Animals were exposed daily either vapors (0.86 g/animal/90 min) or ambient air for 5 days/week over 7 consecutive weeks. At end study period, and inflammatory, oxidative, apoptotic effects vapors,...

10.1002/jat.4286 article EN Journal of Applied Toxicology 2022-01-10

Cardiovascular diseases remain the leading cause of death worldwide. Although major therapeutic progress has been made during past decades, a better understanding underlying mechanisms will certainly help to improve patient's prognosis. In vitro models, particularly adult mouse cardiomyocytes, have largely used; however, their fragility and large size are obstacles use flow cytometry. Conventional techniques, such as cell imaging, require numbers animals time consuming. Here, we described...

10.1152/ajpcell.00393.2019 article EN AJP Cell Physiology 2019-12-26

Ischemic heart diseases are a major cause of death worldwide. Different animal models, including cardiac surgery, have been developed over time. Unfortunately, the surgery models reported to trigger an important inflammatory response that might be effect modifier, where involved molecular processes not fully elucidated yet.We sought perform thorough characterization sham in myocardium and identify interfering reaction order avoid misinterpretation data via systems biology approaches.We...

10.3389/fphys.2019.01370 article EN cc-by Frontiers in Physiology 2019-10-31

10.1016/j.acvdsp.2018.02.022 article EN publisher-specific-oa Archives of Cardiovascular Diseases Supplements 2018-03-23
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