Lipocalin family proteins and their diverse roles in cardiovascular disease

Wang, Xiaohong; Li, Siru; Liu, Yueying; Akbar, Rubab; Gao, Fan

doi:10.1016/j.pharmthera.2023.108385

Cited by 17 publications

(11 citation statements)

References 196 publications

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“…These inhibitors remain viable approaches assuming that the efficacy and safety are comprehensively evaluated. Furthermore, as LCNs have attracted increasing attention in the pathogenesis of diseases such as cardiovascular diseases, age-related brain diseases, and metabolic disorders, ,, more attention should be given to the development of potent LCN inhibitors.…”

Section: Discussionmentioning

confidence: 99%

“…LCNs are a series of extracellular proteins that are approximately 160–180 amino acids in length and most human LCN genes are found on chromosome 9 . LCNs mainly bind various hydrophobic molecules, including fatty acids, steroids, and odorants. , Surprisingly, LCN2 can also bind iron through a siderophore called 2,3-dihydroxybenzoic acid (2,3-DHBA) .…”

Section: Lcnsmentioning

confidence: 99%

“…LCNs have been widely investigated as biomarkers for diseases because of their extracellular properties. − However, since LCNs could bind to specific membrane receptors and form complexes with macromolecules in addition to ligand binding, they have various functions in biological processes that include inflammation, cell proliferation and differentiation, apoptosis, and aging and therefore may directly participate in disease progression. ,, Consequently, developing small inhibitors of LCNs is also a promising strategy for LCN-mediated diseases.…”

Section: Lcnsmentioning

confidence: 99%

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Recent Advances on Small-Molecule Inhibitors of Lipocalin-like Proteins

Chen,

Pan,

Liu

et al. 2024

J. Med. Chem.

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Small-Molecule Inhibitors against RBPs. Synthetic retinoids utilize the ligand-binding characteristics of RBP4 as one type of small-molecule inhibitor. However, nonretinoid ligands can also serve as small-molecule RBP4 inhibitors. Both types of inhibitors target the lipocalin-domain of RBP4 and can therefore be classified into these two groups.Retinoids. N-(4-Hydroxyphenyl)retinamide (also known as fenretinide, Figure 2, compound 1) is a retinol analog that Figure 2. Chemical structures for reported RBP4 small-molecule inhibitors.

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Section: Discussionmentioning

confidence: 99%

Section: Lcnsmentioning

confidence: 99%

Section: Lcnsmentioning

confidence: 99%

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Recent Advances on Small-Molecule Inhibitors of Lipocalin-like Proteins

Chen,

Pan,

Liu

et al. 2024

J. Med. Chem.

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“…Так, NGAL может экспрессироваться в тканях сердца и атеросклеротических бляшках [20]. Его уровни в плазме крови повышаются при ИБС, а также при острой и хронической сердечной недостаточности [21]. Так, в исследовании, выполненным Каретниковой В. Н. и соавт.…”

Section: обсуждение / Discussionunclassified

Relationship between renal damage marker levels and the presence of bleeding in patients with atrial fibrillation and chronic kidney disease receiving rivaroxaban

Shatalova,

Ostroumova,

Korotkova

et al. 2024

GCP

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Relevance. Chronic kidney disease (CKD) is often concomitant pathology in patients with atrial fibrillation (AF). Because of the increased risk of bleeding in patients with AF and CKD while taking anticoagulant therapy, it is necessary to assess new methods for predicting the risk of bleeding when prescribing anticoagulants in this category of patients.Objective. To evaluate the possible relationship between the presence of bleeding in patients with AF and CKD C3–4 receiving rivaroxaban and the level of renal damage markers in urine.Methods. One hundred and thirty-three patients with AF and CKD C3a-C4 aged 52 to 97 years (median age 82 [74;86] years) were included in the study. All patients were assessed for bleeding and excretion of markers of renal damage (albumin; nephrin; neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1)) in with urine have been identified. In addition, the levels of kidney injury markers in the urine of 45 healthy volunteers were analyzed.Results. Urinary NGAL and KIM-1 levels in patients with AF and CKD with a history of bleeding (5.5 [3.81;23.83] ng/ml and 0.68 [0.27;1.10] ng/ml, respectively) were significantly higher than those in patients without bleeding (4.19 [2.22; 15.53] ng/ml, p=0.039, and 0.38 [0.13;0.66] ng/ml, p=0.019, respectively) and healthy subjects (2.6 [1.9;4.3] ng/ml, p<0.001, and 0.21 [0.10;0.69], p=0.003, respectively).Conclusion. Patients with AF and CKD C3a — C4 on rivaroxaban treatment with a history of bleeding have higher urinary excretion of KIM-1 and NGAL.

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“…However, a previous study suggested that activation of zebrafish cardiac Vdr leads to increased proliferation and regeneration of the heart [ 65 ]. Lcn2 encodes lipocalcin 2 and can reduce inflammation by binding to iron carriers [ 66 ]. Several studies suggest that LCN2 protein is a risk factor for atherosclerosis and myocardial ischemic injury [ 67 – 69 ].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of ferroptosis reverses heart failure with preserved ejection fraction in mice

Xiong,

Liu,

Jiang

et al. 2024

J Transl Med

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Background Heart failure with preserved ejection fraction (HFpEF) accounts for approximately 50% of heart failure cases. The molecular mechanisms by which HFpEF leads to impaired diastolic function of the heart have not been clarified, nor have the drugs that target the clinical symptoms of HFpEF patients. Methods HFpEF chip data (GSE180065) was downloaded from the National Center for Biotechnology Information (NCBI) database. Differentially expressed genes (DEGs) were filtered by the limma package in R and processed for GO and KEGG pathway analyses. Then, ferroptosis-related genes in HFpEF were identified by taking the intersection between DEGs and ferroptosis-related genes. CytoHubba and MCODE were used to screen ferroptosis-related hub DEGs in the protein–protein interaction (PPI) network. Establishment of a mouse HFpEF model to validate the transcript levels of ferroptosis-related hub DEGs and ferroptosis-related phenotypes. Transcript levels of ferroptosis-related hub DEGs and HFpEF phenotypic changes in the hearts of HFpEF mice were further examined after the use of ferroptosis inhibitors. Results GO and KEGG enrichment analyses suggested that the DEGs in HFpEF were significantly enriched in ferroptosis-related pathways. A total of 24 ferroptosis-related DEGs were identified between the ferroptosis gene dataset and the DEGs. The established PPI network was further analyzed by CytoHubba and MCODE modules, and 11 ferroptosis-related hub DEGs in HFpEF were obtained. In animal experiments, HFpEF mice showed significant abnormal activation of ferroptosis. The expression trends of the 11 hub DEGs associated with ferroptosis, except for Cdh1, were consistent with the results of the bioinformatics analysis. Inhibition of ferroptosis alters the transcript levels of 11 ferroptosis-related hub DEGs and ameliorates HFpEF phenotypes. Conclusions The present study contributes to a deeper understanding of the specific mechanisms by which ferroptosis is involved in the development of HFpEF and suggests that inhibition of ferroptosis may mitigate the progression of HFpEF. In addition, eleven hub genes were recognized as potential drug binding targets.

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Lipocalin family proteins and their diverse roles in cardiovascular disease

Cited by 17 publications

References 196 publications

Recent Advances on Small-Molecule Inhibitors of Lipocalin-like Proteins

Recent Advances on Small-Molecule Inhibitors of Lipocalin-like Proteins

Relationship between renal damage marker levels and the presence of bleeding in patients with atrial fibrillation and chronic kidney disease receiving rivaroxaban

Inhibition of ferroptosis reverses heart failure with preserved ejection fraction in mice

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