ArticleHypertension (Dallas, Tex. : 1979)2015
Neutrophil Gelatinase-Associated Lipocalin, a Novel Mineralocorticoid Biotarget, Mediates Vascular Profibrotic Effects of Mineralocorticoids.
Article in Hypertension (Dallas, Tex. : 1979), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 98 citations in OpenAlex.
- Serum markers of fibrosis, cardiovascular and all-cause mortality in hemodialysis patients: the AURORA trial.Clinical research in cardiology : official journal of the German Cardiac Society · 2022Trial
- Association Between Plasma Neutrophil Gelatinase-Associated Lipocalin and Cardiac Disease Hospitalizations and Deaths in Older Women.Journal of the American Heart Association · 2019Trial
- Loss of NGAL protects against albumin-induced kidney inflammation and fibrosis.Renal failure · 2026Article
- Adipocyte extracellular vesicles (AdEVs) promote a proinflammatory and profibrotic profile in human renal and endothelial cells in vitro.International journal of obesity (2005) · 2026Article
- Lipocalin-2 in Intracerebral Hemorrhage: Mechanisms, Biomarker Potential, and Therapeutic Targeting.Neuromolecular medicine · 2026Review
- Empagliflozin does not prevent progression of Dent's disease type 1 in a mouse model.Experimental physiology · 2026Article
- Adipokines and Vascular Modulators in CKM: Emerging Biomarkers as Diagnostic and Therapeutic Targets.International journal of molecular sciences · 2025Review
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- Prostaglandin DCells · 2025Article
- Aldosterone in Chronic Kidney Disease.Biomedicines · 2025Review
- Mineralocorticoid receptor activation contributes to intestinal fibrosis through neutrophil gelatinase-associated lipocalin in preclinical models.Nature communications · 2025Article
- Review
- The Review of Current Knowledge on Neutrophil Gelatinase-Associated Lipocalin (NGAL).International journal of molecular sciences · 2023Review
- The Mineralocorticoid Receptor on Smooth Muscle Cells Promotes Tacrolimus-Induced Renal Injury in Mice.Pharmaceutics · 2023Article
- Cardiovascular Disease in Obstructive Sleep Apnea: Putative Contributions of Mineralocorticoid Receptors.International journal of molecular sciences · 2023Review
- Extracellular Vesicles and Hypertension.Advances in experimental medicine and biology · 2023Article
- Sex-dependent expression of neutrophil gelatinase-associated lipocalin in aortic stenosis.Biology of sex differences · 2022Article
- Article
- Nonepithelial mineralocorticoid receptor activation as a determinant of kidney disease.Kidney international supplements · 2022Review
- Mineralocorticoid receptor activation and antagonism in cardiovascular disease: cellular and molecular mechanisms.Kidney international supplements · 2022Review
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the mineralocorticoid receptor has been shown to be deleterious in cardiovascular diseases (CVDs). We have recently shown that lipocalin 2 (Lcn2), or neutrophil gelatinase-associated lipocalin (NGAL), is a primary target of aldosterone/mineralocorticoid receptor in the cardiovascular system. Lcn2 is a circulating protein, which binds matrix metalloproteinase 9 and modulates its stability. We hypothesized that Lcn2 could be a mediator of aldosterone/mineralocorticoid receptor profibrotic effects in the cardiovascular system. Correlations between aldosterone and profibrotic markers, such as procollagen type I N-terminal peptide, were investigated in healthy subjects and subjects with abdominal obesity. The implication of Lcn2 in the mineralocorticoid pathway was studied using Lcn2 knockout mice subjected to a nephrectomy/aldosterone/salt (NAS) challenge for 4 weeks. In human subjects, NGAL/matrix metalloproteinase 9 was positively correlated with plasma aldosterone and fibrosis biomarkers. In mice, loss of Lcn2 prevented the NAS-induced increase of plasma procollagen type I N-terminal peptide, as well as the increase of collagen fibers deposition and collagen I expression in the coronary vessels and the aorta. The lack of Lcn2 also blunted the NAS-induced increase in systolic blood pressure. Ex vivo, treatment of human fibroblasts with recombinant Lcn2 induced the expression of collagen I and the profibrotic galectin-3 and cardiotrophin-1 molecules. Our results showed that Lcn2 plays a key role in aldosterone/mineralocorticoid receptor-mediated vascular fibrosis. The clinical data indicate that this may translate in human patients. Lcn2 is, therefore, a new biotarget in cardiovascular fibrosis induced by mineralocorticoid activation.
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