Zouhair Aherrahrou

ORCID: 0000-0002-1241-8733
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About
Contact & Profiles
Research Areas
  • Atherosclerosis and Cardiovascular Diseases
  • Dermatological and Skeletal Disorders
  • Genetic Associations and Epidemiology
  • Congenital heart defects research
  • Parathyroid Disorders and Treatments
  • Genetic Mapping and Diversity in Plants and Animals
  • Connective tissue disorders research
  • Cardiomyopathy and Myosin Studies
  • Protease and Inhibitor Mechanisms
  • RNA modifications and cancer
  • Protein Tyrosine Phosphatases
  • Cell Adhesion Molecules Research
  • Retinal Diseases and Treatments
  • Heterotopic Ossification and Related Conditions
  • Genetic Neurodegenerative Diseases
  • Renin-Angiotensin System Studies
  • Bone and Dental Protein Studies
  • Cardiac Imaging and Diagnostics
  • Signaling Pathways in Disease
  • Tissue Engineering and Regenerative Medicine
  • Cholesterol and Lipid Metabolism
  • Cardiovascular Function and Risk Factors
  • Receptor Mechanisms and Signaling
  • Hormonal Regulation and Hypertension
  • Galectins and Cancer Biology

University of Lübeck
2015-2025

German Centre for Cardiovascular Research
2016-2025

Institute for Integrative and Experimental Genomics
2013-2024

University of Eastern Finland
2024

Universität Hamburg
2016-2023

University Medical Center Hamburg-Eppendorf
2016-2023

Immungenetics (Germany)
2023

University Hospital Schleswig-Holstein
2005-2020

Deutsches Herzzentrum München
2015

Ministry of Education of the People's Republic of China
2015

Recent genome-wide association (GWA) studies identified 10 chromosomal loci for coronary artery disease (CAD) or myocardial infarction (MI). However, these explain only a small proportion of the genetic variability pertinent diseases. We sought to identify additional CAD/MI by applying three-stage approach.We genotyped n = 1157 MI cases and 1748 controls from population-based study population [German Family Study (GerMIFS) III (KORA)] with SNP arrays. At this first stage, 462 SNPs showed at...

10.1093/eurheartj/ehq405 article EN European Heart Journal 2010-11-18

Background— ADAMTS-7, a member of the disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family, was recently identified to be significantly associated genomewide coronary artery disease. However, mechanisms that link ADAMTS-7 disease risk remain elusive. We have previously demonstrated promotes vascular smooth muscle cell migration postinjury neointima formation via degradation matrix protein cartilage oligomeric protein. Because delayed endothelium repair renders...

10.1161/circulationaha.114.014072 article EN Circulation 2015-02-26

The ADAMTS7 locus was genome-wide significantly associated with coronary artery disease. Lack of the ECM (extracellular matrix) protease ADAMTS-7 (A disintegrin and metalloproteinase-7) shown to reduce atherosclerotic plaque formation. Here, we sought identify molecular mechanisms downstream targets mediating risk atherosclerosis.Targets were identified by high-resolution mass spectrometry plaques from Apoe-/- Apoe-/-Adamts7-/- mice. proteins using solubility profiling. Putative validated...

10.1161/circresaha.123.322737 article EN Circulation Research 2023-09-07

Abnormal mineralization occurs in the context of several common conditions, including advanced age, diabetes, hypercholesterolemia, chronic renal failure, and certain genetic conditions. Metabolic, mechanical, infectious, inflammatory injuries promote ectopic through overlapping yet distinct molecular mechanisms initiation progression. The ABCC6 protein is an ATP-dependent transporter primarily found plasma membrane hepatocytes. exports unknown substrates from liver presumably for systemic...

10.3389/fgene.2012.00289 article EN cc-by Frontiers in Genetics 2012-01-01

Smooth muscle cells (SMCs), which make up the medial layer of arteries, are key cell types involved in cardiovascular disease, leading cause mortality and morbidity worldwide. In response to microenvironment alterations, SMCs dedifferentiate from a contractile synthetic phenotype characterized by an increased proliferation, migration, production ECM (extracellular matrix) components, decreased expression SMC-specific markers. These phenotypic changes result vascular remodeling contribute...

10.1161/atvbaha.123.320274 article EN Arteriosclerosis Thrombosis and Vascular Biology 2024-02-08

Genetic variants of the arachidonic acid monooxygenase CYP4A11 result in decreased synthesis 20-hydroxyeicostatetraenoic and experimental hypertension. Moreover, humans, T8590C polymorphism displayed association with arterial The aim present study was to further investigate this a large population-based sample. Therefore, participants echocardiographic substudy third MONICA (MONitoring trends determinants In CArdiovascular disease) survey (n=1397) were studied by standardized anthropometric,...

10.1161/01.hyp.0000182658.04299.15 article EN mit Hypertension 2005-09-07

Purpose: Multiple evidence lines support Bruch's membrane lipid deposition as a major precursor of soft drusen and age-related macular degeneration including potentially treatable atherosclerosis-like progression in the subretinal pigment epithelium (RPE)-basal lamina space. We evaluated effect anti-inflammatory, antiatherogenic peptide L-4F on aged nonhuman primates dose-escalating study. Methods: Macaca fascicularis ≥20 years age by color fundus photography optical coherence tomography...

10.1167/iovs.18-25786 article EN cc-by-nc-nd Investigative Ophthalmology & Visual Science 2019-02-01

Abstract Background and Aims Chronic inflammation autoimmunity contribute to cardiovascular (CV) disease. Recently, autoantibodies (aAbs) against the CXC-motif-chemokine receptor 3 (CXCR3), a G protein-coupled with key role in atherosclerosis, have been identified. The of anti-CXCR3 aAbs for CV risk disease is unclear. Methods Anti-CXCR3 were quantified by commercially available enzyme-linked immunosorbent assay 5000 participants (availability: 97.1%) population-based Gutenberg Health Study...

10.1093/eurheartj/ehad666 article EN cc-by-nc European Heart Journal 2023-11-06

Abstract Atherosclerosis is the leading cause of death in Western industrial nations. To study etiology plaque progression, atherosclerotic mouse models are widely used. Traditionally, analyzing obtained histological whole slide images Oil Red O-stained aortic roots required manual segmentation. accelerate this process, an artificial intelligence-driven solution proposed that comprises three stages: (1) defining region interest (ROI) root using a YOLOv8l object detector, (2) applying...

10.1038/s41598-025-93967-6 article EN cc-by Scientific Reports 2025-04-23

Atherosclerosis leads to vascular lesions that involve major rearrangements of the proteome, especially extracellular matrix (ECM). Using single aortas from ApoE knock out mice, we quantified formation plaques by single-run, high-resolution mass spectrometry (MS)-based proteomics. To probe localization on a proteome-wide scale employed quantitative detergent solubility profiling. This compartment- and time-resolved resource atherogenesis comprised 5117 proteins, 182 which changed their...

10.1074/mcp.ra117.000315 article EN cc-by Molecular & Cellular Proteomics 2017-12-06

Abstract Genome‐wide association studies (GWAS) have identified coronary artery disease (CAD) susceptibility locus on chromosome 3q22.3. This contains a cluster of several genes that includes muscle rat sarcoma virus ( MRAS ). Common variants are also associated with CAD causing risk factors such as hypertension, dyslipidemia, obesity, and type II diabetes. The gene is an oncogene encodes membrane‐bound small GTPase. It involved in variety signaling pathways, regulating cell differentiation...

10.1002/iub.2805 article EN cc-by-nc-nd IUBMB Life 2024-01-22

We previously demonstrated that mice carrying natural mtDNA variants of the FVB/NJ strain (m.7778 G>T in mt-Atp8 gene mitochondrial complex V), namely C57BL/6 J-mt

10.1016/j.phrs.2024.107231 article EN cc-by-nc-nd Pharmacological Research 2024-05-28

Abstract CYP17A1 is a cytochrome P450 enzyme with 17-alpha-hydroxylase and C17,20-lyase activities. genetic variants are associated coronary artery disease, myocardial infarction visceral subcutaneous fat distribution; however, the underlying pathological mechanisms remain unknown. We aimed to investigate function of its impact on atherosclerosis in mice. At 4–6 months, CYP17A1-deficient mice were viable, KO:Het:WT ratio approximating expected Mendelian 1:2:1. All Cyp17a1 knockout (KO)...

10.1038/s41598-020-65601-0 article EN cc-by Scientific Reports 2020-05-29
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