Susanne Gaul

ORCID: 0000-0003-4780-1844
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About
Contact & Profiles
Research Areas
  • Inflammasome and immune disorders
  • Atherosclerosis and Cardiovascular Diseases
  • Adipokines, Inflammation, and Metabolic Diseases
  • Liver Disease Diagnosis and Treatment
  • RNA Research and Splicing
  • Liver Diseases and Immunity
  • Liver physiology and pathology
  • RNA regulation and disease
  • Viral Infections and Immunology Research
  • Calpain Protease Function and Regulation
  • RNA modifications and cancer
  • Cancer-related molecular mechanisms research
  • Kawasaki Disease and Coronary Complications
  • Immune cells in cancer
  • Immune Response and Inflammation
  • Diabetes and associated disorders
  • Liver Disease and Transplantation
  • Lipid metabolism and disorders
  • Inflammatory Biomarkers in Disease Prognosis
  • Exercise and Physiological Responses
  • Phagocytosis and Immune Regulation
  • Cardiomyopathy and Myosin Studies
  • Alcohol Consumption and Health Effects
  • Pancreatic function and diabetes
  • Cardiovascular Effects of Exercise

Leipzig University
2020-2025

University Hospital Leipzig
2020-2025

Klinik und Poliklinik für Neurologie
2021-2024

Research Institute of Human Morphology
2023

Yonsei University
2023

Ewha Womans University
2023

Severance Hospital
2023

Research Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences
2023

National Medical Research Center of Cardiology
2023

Institute of Experimental Cardiology
2023

Abstract Background and Aims The NOD‐like receptor protein 3 (NLRP3) inflammasome is a central contributor to human acute chronic liver disease, yet the molecular cellular mechanisms by which its activation precipitates injury remain incompletely understood. Here, we present single cell transcriptomic profiling of livers from global transgenic tamoxifen‐inducible constitutively activated Nlrp3 A350V mutant mouse, investigate changes in parenchymal nonparenchymal gene expression that...

10.1002/hep.32320 article EN Hepatology 2022-01-08

Hepatic inflammasome activation is considered a major contributor to liver fibrosis in NASH. Apoptosis signal–regulating kinase 1 (ASK1) an apical mitogen-activated protein that activates hepatic JNK and p38 promote apoptosis, inflammation, fibrosis. The aim of the current study was investigate whether pharmacologic inhibition ASK1 could attenuate driven by using gain-of-function NOD-like receptor 3 (Nlrp3) mutant mice. Tamoxifen-inducible Nlrp3 knock-in (Nlrp3A350V/+CreT-KI) mice WT were...

10.1172/jci.insight.123294 article EN cc-by JCI Insight 2020-01-29

Abstract Alterations of RNA editing that affect the secondary structure RNAs can cause human diseases. We therefore studied in failing hearts. Transcriptome sequencing showed adenosine-to-inosine (A-to-I) was responsible for 80% events myocardium. Failing hearts were characterized by reduced editing. This primarily attributable to Alu elements introns protein-coding genes. In left ventricle, 166 circRNAs upregulated and 7 downregulated compared non-failing controls. Most associated with host...

10.1007/s00395-022-00940-9 article EN cc-by Basic Research in Cardiology 2022-06-23

Males suffer more often from profibrotic changes in liver than females. The underlying mechanism for this sex difference the prevalence and manifestation of Metabolic dysfunction-associated Steatotic Liver Disease (MASLD) is not yet completely known. We studied male female mice that were induced to develop MASLD by consuming a "fast food" diet (FFD) assessed metabolic phenotype as well histology compared them with fed matched control (CD). Our aim was check sex-specific differences...

10.3389/fendo.2025.1567573 article EN cc-by Frontiers in Endocrinology 2025-03-14

Alternative mRNA splicing is a fundamental process to increase the versatility of genome. In humans, cardiac involved in pathophysiology heart failure. Mutations factor RNA binding motif protein 20 (RBM20) cause severe forms cardiomyopathy. To identify novel cardiomyopathy-associated factors, RNA-seq and tissue-enrichment analyses were performed, which identified up-regulated expression Sam68-Like mammalian 2 (SLM2) left ventricle dilated cardiomyopathy (DCM) patients. human heart, SLM2...

10.1016/j.gpb.2021.01.006 article EN cc-by Genomics Proteomics & Bioinformatics 2021-07-15

Atherosclerosis, the main pathology underlying cardiovascular diseases is accelerated in diabetic patients. Genetic mouse models require breeding efforts which are time-consuming and costly. Our aim was to establish a new nongenetic model of inducible metabolic risk factors that mimics hyperlipidemia, hyperglycemia, or both allows detection phenotypic differences dependent on stressor(s).

10.3389/fcvm.2022.813215 article EN cc-by Frontiers in Cardiovascular Medicine 2022-03-08

Inflammation driven by intracellular activation of the NLRP3 inflammasome is involved in pathogenesis a variety diseases including vascular pathologies. Inflammasome specks are released into extracellular compartment from disrupting pyroptotic cells. The potential uptake and function inflammasomes human coronary artery smooth muscle cells (HCASMC) unknown. Fluorescently labeled particles were isolated mutant NLRP3-YFP cell line used to treat primary HCASMC for 4 24 h. Fluorescent...

10.1038/s41598-021-94314-1 article EN cc-by Scientific Reports 2021-07-26

Background: Cardiogenic shock (CS) is characterized by impaired cardiac function, very high mortality, and limited treatment options. The pro-inflammatory signalling during different phases of CS incompletely understood. Methods: We collected serum plasma (N=44) as well freshly isolated peripheral blood mononuclear cells (PBMC, N=7) patients with complicating acute myocardial infarction on admission after revascularization (24h, 48h, 72h) healthy controls (serum N=75; PBMC N=12). Results:...

10.1152/ajpheart.00231.2024 article EN AJP Heart and Circulatory Physiology 2024-08-23

Objectives: The intracellular NLRP3 inflammasome is an important regulator of sterile inflammation. Recent data suggest that particles can be released into circulation. effects exercise on circulating extracellular apoptosis-associated speck-like protein (ASC) and their endothelial cells are not known. Methods: We established a flow cytometric method to quantitate ASC specks in human serum. were quantitated 52 marathon runners 24-72 h before, immediately after, again 24-58 after the run. For...

10.3389/fphys.2022.866938 article EN cc-by Frontiers in Physiology 2022-05-20

Background and aims Transient Elastography is a non-invasive, cost-efficient, non-ionizing, observer-independent reliable method to detect liver fibrosis using Liver Stiffness Measurement (LSM) the degree of fat accumulation in Controlled Attenuation Parameter (CAP). This study derive reference values for both measures from healthy children adolescents. Further, we aim assess potential influence age, sex, puberty, BMI-SDS on CAP LSM. Methods Within LIFE Child study, amongst others,...

10.3389/fendo.2022.1030809 article EN cc-by Frontiers in Endocrinology 2022-09-27

The interleukin-1 (IL-1) family and the NLR pyrin domain-containing 3 (NLRP3) inflammasome contribute to atherogenesis but underlying mechanisms are incompletely understood. Unlike IL-1β, IL-1α is not dependent on NLRP3 exert its pro-inflammatory effects. Here, a non-genetic model was applied characterize role of IL-1α, for pathogenesis atherosclerosis.Atherogenesis induced by gain-of-function PCSK9-AAV8 mutant viruses feeding high-fat western diet (WTD) 12 weeks in C57Bl6/J wildtype mice...

10.3389/fimmu.2023.1252384 article EN cc-by Frontiers in Immunology 2023-08-28

Abstract The NOD-like receptor protein 3 (NLRP3) inflammasome is a central contributor to human acute and chronic liver disease, yet the molecular cellular mechanisms by which its activation precipitates injury remain incompletely understood. Here, we present single cell transcriptomic profiling of livers from global transgenic Tamoxifen-inducible constitutively-activated Nlrp3 A350V mutant mouse, investigate changes in parenchymal non-parenchymal gene expression that accompany inflammation...

10.1101/2021.03.31.437725 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-03-31

Introduction: The versatility of the human genome is increased by process alternative mRNA splicing. Impaired splicing cardiac transcriptome involved in pathophysiology heart failure. Especially, mutations cardiac-specific factors such as RBM20 cause severe forms cardiomyopathy. Aim: We aimed to identify novel cardiomyopathy-associated using a score myocardial tissue specificity including 53 tissues and disease-associated expression changes hearts dilated cardiomyopathy (DCM) patients...

10.1161/circ.144.suppl_1.10966 article EN Circulation 2021-11-16

Abstract Background The interleukin-1 (IL-1) family and the NLR pyrin domain-containing 3 (NLRP3) inflammasome contribute to atherogenesis but underlying mechanism are incompletely understood. Unlike IL-1β, IL-1α is not dependent on NLRP3 exert its pro-inflammatory effects. Here, a non-genetic model was applied characterize role of IL-1α, IL-1β for pathogenesis atherosclerosis. Methods Atherogenesis induced by gain-of-function PCSK9-AAV8 mutant viruses feeding high-fat western diet (WTD) 12...

10.1101/2023.05.31.543077 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-06-04

Abstract Background The role of Interleukin-1 alpha (IL-1α) and beta (IL-1β) in the pathogenesis atherosclerosis vivo has been controversial for years. In contrast to IL-1β, which is dependent on NLR family pyrin domain containing 3 (NLRP3) inflammasome, IL-1α can be tethered plasma membrane (csIL-1α) where it exerts pro-inflammatory effects. We characterised Nlrp3 inflammasome a nongenetic hyperlipidemic mouse model examined function csIL-1α human monocytes. Methods Atherosclerosis was...

10.1093/eurheartj/ehad655.3261 article EN European Heart Journal 2023-11-01

Abstract Background and aims As part of the innate immune response, NLRP3 inflammasomes are involved in process sterile inflammation, IL-1β release key mediators inflammation-related vascular diseases, such as atherosclerosis. Recent data showed existence extracellular released from monocytes during pyroptotic cell death. Their biological function system is still not known. Here, we established a method to detect tested hypothesis that can be internalized by cells, macrophages, endothelial...

10.1093/ehjci/ehaa946.3753 article EN European Heart Journal 2020-11-01

Abstract Background and aims Atherosclerosis, the main pathology underlying cardiovascular diseases is accelerated in diabetic patients (1,2). Genetic mouse models require breeding efforts which are time-consuming costly. Our aim was to establish a new nongenetic model of inducible metabolic risk factors that mimics hyperlipidemia, hyperglycemia, or both allows detection phenotypic differences dependent on stressor(s) any genetic background. Methods results Wild type mice were injected with...

10.1093/eurheartj/ehac544.3078 article EN European Heart Journal 2022-10-01

Abstract Background and purpose Trimethylamine N-oxide (TMAO) is associated with a higher risk of atherosclerotic diseases. However, the underlying molecular mechanisms are not completely understood. Inflammation following endothelial-to-mesenchymal transition (EndMT) – process where endothelial cells (ECs) lose their function phenotype gain mesenchymal character contribute to development atherosclerosis. We therefore aimed investigate potential uptake TMAO into ECs its impact on...

10.1093/eurheartj/ehab724.3396 article EN European Heart Journal 2021-10-01

Abstract Background and purpose Activation of the immune system correlates with severity prognosis patients heart failure (HF). This study aims to identify characterize long non-coding RNAs (lncRNAs) as a potential mechanistic link between pathophysiology HF activation system. Methods results Next-generation sequencing (NGS) studies identified 2.05-fold increase lncRNA Heat4 in blood compared controls, which was validated larger cohort (HF: N=63; Controls: N=38; p<0.05)....

10.1093/eurheartj/ehab724.3298 article EN European Heart Journal 2021-10-01
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