Current and further outlook on the protective potential of Antrodia camphorata against neurological disorders.

Prevalent neurological disorders such as Alzheimer's disease, Parkinson's disease, and stroke are increasingly becoming a global burden as society ages. It is well-known that degeneration and loss of neurons are the fundamental underlying processes, but there are still no effective therapies for these neurological diseases. In recent years, plenty of studies have focused on the pharmacology and feasibility of natural products as new strategies for the development of drugs that target neurological disorders. Antrodia camphorata has become one of the most promising candidates, and the crude extracts and some active metabolites of it have been reported to play various pharmacological activities to alleviate neurological symptoms at cellular and molecular levels. This review highlights the current evidence of Antrodia camphorata against neurological disorders, including safety evaluation, metabolism, blood-brain barrier penetration, neuroprotective activities, and the potential on regulating the gut-microbiome-brain axis. Furthermore, potential strategies to resolve problematic issues identified in previous studies are also discussed. We aim to provide an overview for the ongoing development and utilization of Antrodia camphorata in cerebral neuropathology.

Characterization of the complete mitochondrial genome of Ergasilus anchoratus Markevich, 1946 (Ergasilidae) and phylogeny of Copepoda.

The mitochondrial (mt) genome can provide data for phylogenetic analyses and evolutionary biology. Herein, we sequenced and annotated the complete mt genome of Ergasilus anchoratus. This mt genome was 13852 bp long and comprised 13 protein-coding genes (PCGs), 22 tRNAs and 2 rRNAs. All PCGs used the standard ATN start codons and complete TAA/TAG termination codons. A majority of tRNA genes exhibited standard cloverleaf secondary structures, with the exception of one tRNA that lacked the TψC arm (trnC), and three tRNAs that lacked the DHU arm (trnR, trnS1 and trnS2). Phylogenetic analyses conducted using Bayesian inference (BI) and maximum likelihood (ML) methods both supported Ergasilidae as a monophyletic family forming a sister group to Lernaea cyprinacea and Paracyclopina nana. It also supported the monophyly of orders Calanoida, Cyclopoida, and Siphonostomatoida; and the monophyly of families Harpacticidae, Ergasilidae, Diaptomidae, and Calanidae. The gene orders of E. anchoratus and Sinergasilus undulatus were identical, which represents the first instance of two identical gene orders in copepods. More mt genomes are needed to better understand the phylogenetic relationships within Copepoda in the future.

SLC25A3 negatively regulates NLRP3 inflammasome activation by restricting the function of NLRP3.

The NACHT, leucine-rich repeat, and pyrin domains-containing protein 3 (collectively known as NLRP3) inflammasome activation plays a critical role in innate immune and pathogenic microorganism infections. However, excessive activation of NLRP3 inflammasome will lead to cellular inflammation and tissue damage, and naturally it must be precisely controlled in the host. Here, we discovered that solute carrier family 25 member 3 (SLC25A3), a mitochondrial phosphate carrier protein, plays an important role in negatively regulating NLRP3 inflammasome activation. We found that SLC25A3 could interact with NLRP3, overexpression of SLC25A3 and knockdown of SLC25A3 could regulate NLRP3 inflammasome activation, and the interaction of NLRP3 and SLC25A3 is significantly boosted in the mitochondria when the NLRP3 inflammasome is activated. Our detailed investigation demonstrated that the interaction between NLRP3 and SLC25A3 disrupted the interaction of NLRP3-NEK7, promoted ubiquitination of NLRP3, and negatively regulated NLRP3 inflammasome activation. Thus, these findings uncovered a new regulatory mechanism of NLRP3 inflammasome activation, which provides a new perspective for the therapy of NLRP3 inflammasome-associated inflammatory diseases.

Global m6A methylation and gene expression patterns in human microglial HMC3 cells infected with HIV-1.

N6-methyladenosine (m6A) methylation of human immunodeficiency virus type 1 (HIV-1) RNA regulates viral replication, and the m6A of host RNA is affected by HIV-1 infection, but its global pattern and function are still unclear. In this study, we report that the number and position of m6A peaks in huge genes of human microglial HMC3 cells were modulated by a single cycle HIV-1 pseudotyped with VSV-G envelope glycoprotein infection using methylated RNA immunoprecipitation sequencing (MeRIP-seq). A conjoint analysis of MeRIP-seq and high-throughput sequencing for mRNA (RNA-seq) explored four groups of clearly classified genes, including 45 hyper-up (m6A-mRNA), 45 hyper-down, 120 hypo-up, and 54 hypo-down genes, in HIV-1 infected cells compared to uninfected ones. KEGG pathway analysis showed that these genes were mainly enriched in the Wnt and TNF signaling pathway, and cytokine-cytokine receptor interaction, which might be related to the immune response in HMC3 cells. And some of these genes might be associated with the pathway of axon guidance and neuroactive ligan-receptor interaction, which affect the neuronal state. However, the cognitive disorders caused by HIV-1 is associated with inflammatory changes that have not yet been well clarified. Furthermore, we confirmed the expression and m6A levels of four genes using RT-PCR and MeRIP-qPCR. Similar to the sequencing results, the expressions of these genes were significantly upregulated by HIV-1 infection. And the m6A level of IL-6 was downregulated, and those of HLA-B, CFB, and OLR1 were upregulated. These results suggest that HIV-1-induced changes in gene expression may be achieved through the regulation of methylation. Our study revealed the global m6A methylation and gene expression patterns under HIV-1 infection in human microglia, which might provide clues for understanding the interaction between HIV-1 and host cells and the cognitive disorders caused by HIV-1.

Correction: Sun et al. Ergosterol Isolated from Antrodia camphorata Suppresses LPS-Induced Neuroinflammatory Responses in Microglia Cells and ICR Mice. Molecules 2023, 28, 2406.

The original version of this article unfortunately contains an error in Figures 4B,C,H-J and 5C,D [...].

Antibacterial chitosan-based composite sponge with synergistic hemostatic effect for massive haemorrhage.

Uncontrollable acute bleeding and wound infection pose significant challenges in emergency treatment and surgical operations. Therefore, the research and development of highly efficient antibacterial hemostatic agents are of great importance in reducing the mortality rate among patients with massive hemorrhage. In this study, we utilized hydrophobically modified chitosan (HM-CS) and gallic acid chitosan (GA-CS) to create a composite sponge (HM/GA-CS) that exhibits complementary advantages. The composite sponge combines the alkyl chain and polyphenol structure, allowing it to adsorb blood cells and plasma proteins simultaneously. This synergistic effect was confirmed through various tests, including blood cell adhesion, plasma protein barrier behavior, and in vitro hemostatic testing. Furthermore, experiments conducted on a rat liver injury model demonstrated that the composite sponge achieved rapid coagulation within 52 s, resulting in significantly lower bleeding volume compared with traditional gauze. In addition, the incorporation of GA-CS into HM-CS enhanced the antibacterial properties of the composite sponge. The antibacterial rate of the composite sponge against Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) reached 100 % and 98.2 %, respectively. To evaluate its biocompatibility, the composite sponge underwent blood compatibility and cell activity tests, confirming its suitability. The HM/GA-CS sponge holds promising applications in managing cases of massive hemorrhage.

A novel scatterplot-based method to detect copy number variation (CNV).

Objective: Most methods to detect copy number variation (CNV) have high false positive rates, especially for small CNVs and in real-life samples from clinical studies. In this study, we explored a novel scatterplot-based method to detect CNVs in microarray samples. Methods: Illumina SNP microarray data from 13,254 individuals were analyzed with scatterplots and by PennCNV. The data were analyzed without the prior exclusion of low-quality samples. For CNV scatterplot visualization, the median signal intensity of all SNPs located within a CNV region was plotted against the median signal intensity of the flanking genomic region. Since CNV causes loss or gain of signal intensities, carriers of different CNV alleles pop up in clusters. Moreover, SNPs within a deletion are not heterozygous, whereas heterozygous SNPs within a duplication show typical 1:2 signal distribution between the alleles. Scatterplot-based CNV calls were compared with standard results of PennCNV analysis. All discordant calls as well as a random selection of 100 concordant calls were individually analyzed by visual inspection after noise-reduction. Results: An algorithm for the automated scatterplot visualization of CNVs was developed and used to analyze six known CNV regions. Use of scatterplots and PennCNV yielded 1019 concordant and 108 discordant CNV calls. All concordant calls were evaluated as true CNV-findings. Among the 108 discordant calls, 7 were false positive findings by the scatterplot method, 80 were PennCNV false positives, and 21 were true CNVs detected by the scatterplot method, but missed by PennCNV (i.e., false negative findings). Conclusion: CNV visualization by scatterplots allows for a reliable and rapid detection of CNVs in large studies. This novel method may thus be used both to confirm the results of genome-wide CNV detection software and to identify known CNVs in hitherto untyped samples.

Hydrophobically modified hydrogel with enhanced tissue adhesion and antibacterial capacity for wound healing.

The increasing emergence of drug-resistant bacteria and bacteria-infected wounds highlights the urgent need for new kinds of antibacterial wound dressing. Herein, we reported a novel bio-adhesive and antibacterial hydrogel consisting of hydrophobically modified gelatin, oxidized konjac glucomannan, and dopamine. This kind of functional hydrogel was endowed with developed stability in a liquid environment and strong tissue adhesion, even much higher than the commercial fibrin glue to wounds. The excellent bacteria-killing efficiency of hydrophobically modified hydrogel against S. aureus and E. coli was verified, as well as the low hemolysis ratio against erythrocytes in vitro. The hydrogel also exhibited good cytocompatibility in terms of supporting cell proliferation. Most importantly, these abovementioned properties could be customized by altering the substitution degree of hydrophobic groups during manufacturing, demonstrating its great potential in biomedical fields such as tissue adhesive and wound dressing.

SARS-CoV-2 Nsp8 induces mitophagy by damaging mitochondria.

Autophagy plays an important role in the interaction between viruses and host cells. SARS-CoV-2 infection can disrupt the autophagy process in target cells. However, the precise molecular mechanism is still unknown. In this study, we discovered that the Nsp8 of SARS-CoV-2 could cause an increasing accumulation of autophagosomes by preventing the fusion of autophagosomes and lysosomes. From further investigation, we found that Nsp8 was present on mitochondria and can damage mitochondria to initiate mitophagy. The results of experiments with immunofluorescence revealed that Nsp8 induced incomplete mitophagy. Moreover, both domains of Nsp8 orchestrated their function during Nsp8-induced mitophagy, in which the N-terminal domain colocalized with mitochondria and the C-terminal domain induced auto/mitophagy. This novel finding expands our understanding of the function of Nsp8 in promoting mitochondrial damage and inducing incomplete mitophagy, which helps us to understand the etiology of COVID-19 as well as open up new pathways for creating SARS-CoV-2 treatment methods.

Protocatechualdehyde-ferric iron tricomplex embedded gelatin hydrogel with adhesive, antioxidant and photothermal antibacterial capacities for infected wound healing promotion.

Because of the indiscriminate use of antibiotics and the increasing threat of drug-resist bacteria, there is an urgent need to develop novel antibacterial strategies to combat infected wounds. In this work, stable tricomplex molecules (PA@Fe) assembled by protocatechualdehyde (PA) and ferric iron (Fe) were successfully synthesized and then embedded in the gelatin matrix to obtain a series of Gel-PA@Fe hydrogels. The embedded PA@Fe served as a crosslinker to improve the mechanical, adhesive and antioxidant properties of hydrogels through coordination bonds (catechol-Fe) and dynamic Schiff base bonds, meanwhile acting as a photothermal agent to convert near-infrared (NIR) light into heat to kill bacteria effectively. Importantly, in vivo evaluation through an infected full-thickness skin wound mice model revealed that Gel-PA@Fe hydrogel developed collagen deposition, and accelerated reconstruction of wound closure, indicating great potential of Gel-PA@Fe hydrogel in promoting the healing process of infected full-thickness wounds.

Gut microbiome alterations in patients with COVID-19-related coagulopathy.

COVID-19 is characterized by a predominantly prothrombotic state, which underlies severe disease and poor outcomes. Imbalances of the gut microbiome have been linked with abnormal hemostatic processes. Understanding the relationship between the gut microbiome and abnormal coagulation parameters in COVID-19 could provide a novel framework for the diagnosis and management of COVID-related coagulopathies (CRC). This cross-sectional study used shotgun metagenomic sequencing to examine the gut microbiota of patients with CRC (n = 66) and compared it to COVID control (CCs) (n = 27) and non-COVID control (NCs) (n = 22) groups. Three, 1, and 3 taxa were found enriched in CRCs, CCs, and NCs. Next, random forest models using 7 microbial biomarkers and differential clinical characteristics were constructed and achieved strong diagnostic potential in distinguishing CRC. Specifically, the most promising biomarker species for CRC were Streptococcus thermophilus, Enterococcus faecium, and Citrobacter portucalensis. Conversely, Enterobacteriaceae family and Fusicatenibacter genus are potentially protective against CRC in COVID patients. We further identified 4 species contributing to 20 MetaCyc pathways that were differentially abundant among groups, with S. thermophilus as the main coding species in CRCs. Our findings suggest that the alterations of gut microbiota compositional and functional profiles may influence the pathogenesis of CRC and that microbiota-based diagnosis and treatment could potentially benefit COVID patients in preventing and alleviating thrombosis-related clinical outcomes.

Ethyl-acetate fraction from a cinnamon-cortex extract protects pancreatic ß-cells from oxidative stress damage.

Background: The pathogenesis of diabetes mellitus is mediated mainly by oxidative stress produced by damaged pancreatic ß-cells. We identified that an ethyl-acetate fraction (EA) from a cinnamon-cortex extract (CCE) is rich in flavonoid, and showed no toxicity to ß cells. Objective: In this study, we evaluated the pharmacologic activities of EA on pancreatic ß cells using a model of oxidative stress induced by H2O2 or alloxan. Results: The results showed that EA could significantly reduce reactive oxygen (ROS) accumulation to improve the survival of cells. Western blot showed that EA treatment upregulated expression of nuclear factor erythroid 2 related factor 2, heme oxygenase-1, and gamma glutamylcysteine synthetase. The same model study found that EA also can protect ß cells against the apoptosis induced by oxidative stress. Furthermore, EA can enhance insulin secretion in rat and mouse ß cell lines treated or not with alloxan or H2O2. The expression of the insulin transcription factor PDX-1 increased in an EA concentration-dependent manner. At last, the major functional compounds of EA analysis showed that three compounds, cinnamyl alcohol, coumarin, and cinnamic acid, had similar effects as EA. Conclusions: In sum, our data suggested that EA fraction from CCE can protect ß cells from oxidative stress, and increase insulin secretion to improve the function of ß cells. This function might be due to these three compounds found in EA. Our findings provide a theoretical basis and functional molecules for the use of CCE against diabetes mellitus.

Ergosterol Isolated from Antrodia camphorata Suppresses LPS-Induced Neuroinflammatory Responses in Microglia Cells and ICR Mice.

Inflammation caused by microglial activation is important in neurodegenerative diseases. In this research, we tried to identify safe and effective anti-neuroinflammatory agents by screening a natural compounds library and found that Ergosterol can inhibit the nuclear factor kappa-light-chain enhancer of the activated B cells (NF-κB) pathway induced by lipopolysaccharide (LPS) in microglia cells. Ergosterol has been reported to be an effective anti-inflammatory agent. Nevertheless, the potential regulatory role of Ergosterol in neuroinflammatory responses has not been fully investigated. We further investigated the mechanism of Ergosterol that regulates LPS-induced microglial activation and neuroinflammatory reactions both in vitro and in vivo. The results showed that Ergosterol can significantly decrease the pro-inflammatory cytokines induced by LPS in BV2 and HMC3 microglial cells, possibly by inhibiting the NF-κB, protein kinase B (AKT), and mitogen-activated protein kinase (MAPK) signaling pathways. In addition, we treated Institute of Cancer Research (ICR) mice with a safe concentration of Ergosterol following LPS injection. Ergosterol treatment significantly decreased microglial activation-associated ionized calcium-binding adapter molecule-1 (IBA-1), NF-κB phosphorylation, and pro-inflammatory cytokine levels. Moreover, Ergosterol pretreatment clearly reduced LPS-induced neuron damage by restoring the expression of synaptic proteins. Our data may provide insight into possible therapeutic strategies for neuroinflammatory disorders.

Two Resveratrol Oligomers Inhibit Cathepsin L Activity to Suppress SARS-CoV-2 Entry.

Cell entry of severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) depends on specific host cell proteases, which are the key targets for preventing and treating viral infections. Herein, we describe miyabenol C and trans-ε-viniferin, two resveratrol oligomers that specifically inhibit SARS-CoV-2 entry by targeting host protease cathepsin L. Several cell-based assays were used to demonstrate the effect of resveratrol oligomers, and their target was identified via screening of antiviral targets. Molecular docking analysis suggested that the oligomers could occupy the active cavity of cathepsin L. The surface plasmon resonance assay showed that the equilibrium dissociation constant (KD) values of miyabenol C-cathepsin L and trans-ε-viniferin-cathepsin L were 5.54 and 8.54 µM, respectively, indicating their excellent binding ability for cathepsin L. Our study demonstrated the potential application of resveratrol oligomers as lead compounds in controlling SARS-CoV-2 infection by targeting cathepsin L.

HIV-1 Infection Promotes Cholesterol Aggregation by Inducing miR-33b-5p to Suppress ABCA1 Expression.

MicroRNAs play an important role in the interaction between viruses and hosts. In this study, we found that the expression level of miR-33b-5p was markedly increased in human immunodeficiency virus type 1 (HIV-1)-infected cell lines and the serum of person with HIV-1. Further investigation revealed that the level of ATP-binding cassette transporter (ABCA1), which transports cholesterol between intracellular and extracellular compartments to maintain cholesterol homeostasis, was reduced in HIV-1-infected target cells, as the target gene of miR-33b-5p. Furthermore, HIV-1 infection stimulated abnormal lipid transport in macrophages, resulting in lipid accumulation in cells. These changes can be reversed by an miR-33b-5p inhibitor. We discovered a mechanism through which HIV-1 infection caused miR-33b-5p to target ABCA1 and caused aberrant lipid transport, providing a novel method for diagnosing and treating poor lipid metabolism in person with HIV-1.

Gut microbiota mediated the individualized efficacy of Temozolomide via immunomodulation in glioma.

BACKGROUND: Temozolomide (TMZ) is the preferred chemotherapy strategy for glioma therapy. As a second-generation alkylating agent, TMZ provides superior oral bio-availability. However, limited response rate (less than 50%) and high incidence of drug resistance seriously restricts TMZ's application, there still lack of strategies to increase the chemotherapy sensitivity. METHODS: Luci-GL261 glioma orthotopic xenograft model combined bioluminescence imaging was utilized to evaluate the anti-tumor effect of TMZ and differentiate TMZ sensitive (S)/non-sensitive (NS) individuals. Integrated microbiomics and metabolomics analysis was applied to disentangle the involvement of gut bacteria in TMZ sensitivity. Spearman's correlation analysis was applied to test the association between fecal bacteria levels and pharmacodynamics indices. Antibiotics treatment combined TMZ treatment was used to confirm the involvement of gut microbiota in TMZ response. Flow cytometry analysis, ELISA and histopathology were used to explore the potential role of immunoregulation in gut microbiota mediated TMZ response. RESULTS: Firstly, gut bacteria composition was significantly altered during glioma development and TMZ treatment. Meanwhile, in vivo anti-cancer evaluation suggested a remarkable difference in chemotherapy efficacy after TMZ administration. Moreover, 16s rRNA gene sequencing and non-targeted metabolomics analysis revealed distinct different gut microbiota and immune infiltrating state between TMZ sensitive and non-sensitive mice, while abundance of differential gut bacteria and related metabolites was significantly correlated with TMZ pharmacodynamics indices. Further verification suggested that gut microbiota deletion by antibiotics treatment could accelerate glioma development, attenuate TMZ efficacy and inhibit immune cells (macrophage and CD8α+ T cell) recruitment. CONCLUSIONS: The current study confirmed the involvement of gut microbiota in glioma development and individualized TMZ efficacy via immunomodulation, hence gut bacteria may serve as a predictive biomarker as well as a therapeutic target for clinical TMZ application.

The KIR2DL2/HLA-C1C1 Gene Pairing Is Associated With an Increased Risk of SARS-CoV-2 Infection.

SARS-CoV-2 is the causative agent for the global COVID-19 pandemic; however, the interaction between virus and host is not well characterized. Natural killer cells play a key role in the early phase of the antiviral response, and their primary functions are dependent on signaling through the killer cell immunoglobulin-like receptor (KIR). This study measured the association between KIR/HLA class I ligand pairings and the occurrence and development of COVID-19. DNA of blood samples from 257 COVID-19 patients were extracted and used to detect KIR and HLA-C gene frequencies using single strain sequence-specific primer (SSP) PCR. The frequency of these genes was compared among 158 individuals with mild COVID-19, 99 with severe disease, and 98 healthy controls. The frequencies of KIR2DL2 (P=0.04, OR=1.707), KIR2DS3 (P=0.047, OR=1.679), HLA-C1C1 (P<0.001, OR=3.074) and the KIR2DL2/HLA-C1C1 pairing (P=0.038, OR=2.126) were significantly higher in the COVID-19 patients than the healthy controls. At the same time, the frequency of KIR2DL3+KIR2DL2-/HLA-C1+Others+ was lower in COVID-19 patients than in healthy individuals (P=0.004, OR=0.477). These results suggest that the protective effect of KIR2DL3 against SARS-CoV-2 infection is related to the absence of the KIR2DL2 gene. This study found no correlation between the frequencies of these genes and COVID-19 pathogenesis. Global statistical analysis revealed that the incidence of COVID-19 infection was higher in geographic regions with a high frequency of KIR2DL2. Together these results suggest that the KIR2DL2/HLA-C1C1 gene pairing may be a risk factor for SARS-CoV-2 infection.

Multiple Arterial Dissections and Connective Tissue Abnormalities.

BACKGROUND: Although patients with multiple arterial dissections in distinct arterial regions rarely present with known connective tissue syndromes, we hypothesized that mild connective tissue abnormalities are common findings in these patients. METHODS: From a consecutive register of 322 patients with cervical artery dissection (CeAD), we identified and analyzed 4 patients with a history of additional dissections in other vascular beds. In three patients, dermal connective tissue was examined by electron microscopy. DNA from all four patients was studied by whole-exome sequencing and copy number variation (CNV) analysis. RESULTS: The collagen fibers of dermal biopsies were pathologic in all three analyzed patients. One patient carried a CNV disrupting the COL3A1 and COL5A2 genes (vascular or hypermobility type of Ehlers-Danlos syndrome), and another patient a CNV in MYH11 (familial thoracic aortic aneurysms and dissections). The third patient carried a missense substitution in COL5A2. CONCLUSION: Three patients showed morphologic alterations of the dermal connective tissue, and two patients carried pathogenic variants in genes associated with arterial connective tissue dysfunction. The findings suggest that genetic testing should be recommended after recurrent arterial dissections, independently of apparent phenotypical signs of connective tissue disorders.

CD56dim NK Cell is an Important Factor in T Cell Depletion of cART-Treated AIDS Patients.

Purpose: To investigate factors involved in T-cell depletion in combination antiretroviral therapy (cART)-treated human immunodeficiency virus 1 (HIV-1)-positive patients. Patients and Methods: 29 HIV-1-positive patients were enrolled. The CD4+, CD8+ T cell subsets and CD56dim NK cells were detected by flow cytometry. The concentrations of cytokines were measured by enzyme-linked immunosorbent assay. Extraction, amplification, and viral load quantification of specimens were performed using the Roche Cobas Ampliprep/Cobas TaqMan HIV-1 test. Results: Compared with IR group, the total number of red blood cells (RBCs) and lymphocytes (LCs) in INR group was significantly reduced, and there was a significant positive correlation between the number of RBCs and that of LCs. The overall production rates of T cells-related cytokines were lower in INR group. However, the cell-surface expression of programmed death-1 (PD-1) on CD4+ T and CD8+ T cells were markedly elevated in INR group. Moreover, it was found that the proportion and the killing ability of CD56dim NK cells significantly increased in INR patients, and significantly correlated with apoptosis of T lymphocytes. Conclusion: A poor immune reconstitution in HIV-positive patients might result from multiple factors, including bone marrow suppression, high PD-1 expression on the surface of CD4+ T cells, and over-activation of T and NK cells. Besides, the activity of NK cells and RBCs count might be important auxiliary indicators for immune reconstitution and provided a reliable guidance for developing strategies to improve immune reconstitution.

Genetic Variation in LRP1 Associates with Stanford Type B Aortic Dissection Risk and Clinical Outcome.

Genetic variation in LRP1 (low-density lipoprotein receptor-related protein 1) was reported to be associated with thoracic aortic dissections and aneurysms. The aims of this study were to confirm this association in a prospective single-center patient cohort of patients with acute Stanford type B aortic dissections (STBAD) and to assess the impact of LRP1 variation on clinical outcome. The single nucleotide variation (SNV) rs11172113 within the LRP1 gene was genotyped in 113 STBAD patients and 768 healthy control subjects from the same population. The T-allele of rs11172113 was more common in STBAD patients as compared to the reference group (72.6% vs. 59.6%) and confirmed to be an independent risk factor for STBAD (p = 0.002) after sex and age adjustment in a logistic regression model analyzing diabetes, smoking and hypertension as additional risk factors. Analysis of clinical follow-up (median follow-up 2.0 years) revealed that patients with the T-allele were more likely to suffer aorta-related complications (T-allele 75.6% vs. 63.8%; p = 0.022). In this study sample of STBAD patients, variation in LRP1 was an independent risk factor for STBAD and affected clinical outcome.