Fredrik Landfors

ORCID: 0000-0002-5695-2276
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About
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Research Areas
  • Diabetes, Cardiovascular Risks, and Lipoproteins
  • Lipid metabolism and disorders
  • Cancer-related molecular mechanisms research
  • Lipid metabolism and biosynthesis
  • Adipokines, Inflammation, and Metabolic Diseases
  • Cardiovascular Function and Risk Factors
  • Lipoproteins and Cardiovascular Health
  • Cardiovascular Disease and Adiposity
  • Nuclear Receptors and Signaling
  • Hormonal Regulation and Hypertension
  • Liver Disease Diagnosis and Treatment
  • Diabetes and associated disorders
  • Thermoregulation and physiological responses
  • Adipose Tissue and Metabolism
  • Atherosclerosis and Cardiovascular Diseases
  • Cardiac Fibrosis and Remodeling
  • Respiratory Support and Mechanisms

Umeå University
2019-2025

Lipigon Pharmaceuticals (Sweden)
2024

University Hospital of Umeå
2024

Abstract Aims APOC3, ANGPTL3, and ANGPTL4 are circulating proteins that actively pursued as pharmacological targets to treat dyslipidaemia reduce the risk of atherosclerotic cardiovascular disease. Here, we used human genetic data compare predicted therapeutic adverse effects inactivation. Methods results We conducted drug-target Mendelian randomization analyses using variants in proximity genes associated with protein levels drug targets. obtained exposure outcome from large-scale...

10.1093/ehjopen/oeae035 article EN cc-by European Heart Journal Open 2024-04-30

Abstract Imaging-defined atherosclerosis represents an intermediate phenotype of atherosclerotic cardiovascular disease (ASCVD). Genome-wide association studies (GWAS) on directly measured coronary plaques using computed tomography angiography (CCTA) are scarce. In the so far largest population-based cohort with CCTA data, we performed a GWAS plaque burden as determined by segment involvement score (SIS) in 24,811 European individuals. We identified 20 significant independent genetic markers...

10.1038/s41467-025-57457-7 article EN cc-by Nature Communications 2025-03-31

Angiopoietin-like proteins, ANGPTL3, ANGPTL4, and ANGPTL8, are involved in regulating plasma lipids. In vitro animal-based studies point to LPL endothelial lipase (EL, LIPG) as key targets of ANGPTLs. To examine the ANGPTL mechanisms for lipid modulation humans, we pursued a genetic mimicry analysis enhancing or suppressing variants LPL, LIPG, C hepatic type (LIPC), ANGPTL8 genes using data on 248 metabolic parameters derived from over 110,000 nonfasted individuals UK Biobank validated...

10.1016/j.jlr.2022.100313 article EN cc-by Journal of Lipid Research 2022-11-11

LPL is a key player in plasma triglyceride metabolism. Consequently, regulated by several proteins during synthesis, folding, secretion, and transport to its site of action at the luminal side capillaries, as well catalytic reaction. Some are known, whereas others have been identified but still not fully understood. We set out study effects natural variations levels all known regulators on activity purified added samples fasted taken from 117 individuals. The enzymatic was measured 25°C...

10.1016/j.jlr.2021.100144 article EN cc-by Journal of Lipid Research 2021-10-26

ABSTRACT Background and Aims APOC3, ANGPTL3, ANGPTL4 are circulating proteins that actively pursued as pharmacological targets to treat dyslipidemia reduce the risk of atherosclerotic cardiovascular disease. Here, we used human genetic data compare predicted therapeutic adverse effects inactivation. Methods We conducted drug-target Mendelian randomization analyses using variants in proximity genes associated with protein levels drug targets. obtained exposure outcome from large-scale...

10.1101/2024.01.23.24301541 preprint EN cc-by-nc-nd medRxiv (Cold Spring Harbor Laboratory) 2024-01-23

Background: Genetic studies consistently demonstrate that individuals born with reduced Cholesteryl Ester Transfer Protein (CETP) activity experience lower rates of atherosclerotic vascular disease throughout their lives. In contrast, short-term randomized controlled trials CETP inhibitors have yielded mixed results, only one four reporting a reduction in clinical events. Several theories been proposed to explain this discrepancy, but none fully account for the central mechanism...

10.1101/2024.12.02.24318306 preprint EN cc-by medRxiv (Cold Spring Harbor Laboratory) 2024-12-03

Patients at a high risk for sudden cardiac death (SCD) without previous history of cardiovascular disease remain challenge to identify. Atherosclerosis and prothrombotic states involve inflammation non-cardiac tissue damage that may play active roles in SCD development. Therefore, we hypothesized circulating proteins implicated are linked the future SCD. We conducted prospective nested case-control study cases with verified myocardial infarction (N = 224) matched controls 224), aged 60 ± 10...

10.3390/ijms231810251 article EN International Journal of Molecular Sciences 2022-09-06
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