Targeting Leukotrienes as a Therapeutic Strategy to Prevent Comorbidities Associated with Metabolic Stress

Ramalho, Theresa; Pereira, Nayara; Brandt, Stephanie; Serezani, Carlos Henrique

doi:10.1007/978-3-030-50621-6_4

Cited by 3 publications

(4 citation statements)

References 120 publications

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“…The cannabinoid receptor agonist, Lenabasum can reduce IL-6 transcription in macrophages in vitro (61), suggesting direct effects on the inflammatory potential of these cells. It had modest clinical effects, but exhibited a significant reduction in sputum interleukin-8 content (61).…”

Section: Drugs Targeting Cf Inflammation Statusmentioning

confidence: 99%

“…Pathogens that are rarer but more difficult to treat, like the non-tuberculous mycobacterium (NTM). M. abscessus (61,62), can cause acute and chronic problems that have a negative impact on the prognosis of infected individuals. A wide range of medications, including antibiotic adjuvants, biofilmtargeted strategies, and bacteriophages, are waiting to be approved for use in pediatric pathology related to CF (63).…”

Section: Drugs Targeting Cf Inflammation Statusmentioning

confidence: 99%

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Cystic fibrosis management in pediatric population—from clinical features to personalized therapy

Azoicai,

Lupu,

Trandafir

et al. 2024

Front. Pediatr.

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Cystic fibrosis (CF) is an autosomal recessive disease caused by mutations of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). In 1949, it's been identified as a monogenic disease and was thought to primarily affect individuals of Northern European descent. It was the most prevalent autosomal recessive disease that shortens life. With the availability of multiple testing methodologies nowadays, there is a chance to create novel and enhanced treatment options. Even in the absence of a high sweat chloride test (SCT) result, the discovery of two causal mutations is diagnostic for cystic fibrosis (CF). For a CF diagnosis, however, at least two positive E sweat chloride tests are still required. In order to achieve early and active intervention to manage cystic fibrosis (CF) and its comorbidities, treatment regimens for pediatric patients should be evaluated, improved, and closely monitored. New developments in the treatment of cystic fibrosis (CF) have led to the development of medications derived from molecules that target the pathogenetic pathway of the illness. These options are very efficient and allow pediatric patients to receive individualized care. However, in order to better direct patient care and enhance patient outcomes, it is crucial to research uncommon CF mutations, which can provide crucial information about the prognosis of the disease and the relationships between genotype and phenotype. To ensure the success of creating novel, safer, and more efficient treatment approaches, a deeper understanding of the pathogeny of the illness is required. In the age of customized medicine, genetic research will be essential to improving patient care and quality of life for those with uncommon mutations.

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Section: Drugs Targeting Cf Inflammation Statusmentioning

confidence: 99%

Section: Drugs Targeting Cf Inflammation Statusmentioning

confidence: 99%

Cystic fibrosis management in pediatric population—from clinical features to personalized therapy

Azoicai,

Lupu,

Trandafir

et al. 2024

Front. Pediatr.

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“…In humans, saturated FAs (palmitic acid, stearic acid) are de novo synthesized by elongation. However, polyunsaturated fatty acids (PUFAs: i.e., linoleic acid, LA (18:2, ∆ 9,12 , ω-6); arachidonic acid, AA (20:4, ∆ 5,8,11,14 , ω-6); alpha-linolenic acid, ALA (18:3, ∆ 9,12,15 , ω-3); docosapentaenoic acid, DPA (22:5, ∆ 4,7,10,13,16 , ω-3); docosahexaenoic acid, DHA (22:6, ∆ 4,7,10,13,16,19 , ω-3); eicosapentaenoic acid, EPA (20:5, ∆ 5,8,11,14,17 , ω-3)) are not produced directly due to the absence of desaturases that introduce a double bond into FAs distal to the ∆9 position. Thus, dietary PUFAs are essential for human beings.…”

Section: Introductionmentioning

confidence: 99%

“…PGs, LTs, and other lipid mediators play physiological and pathophysiological roles via cognate G protein-coupled receptors (GPCRs) [ 7 ]. Because these lipid mediators show pleiotropic functions in a variety of diseases [ 8 , 9 , 10 ], drugs targeting this signaling have been developed, such as non-steroidal anti-inflammatory drugs (NSAIDs; aspirin, indomethacin, and diclofenac for treatment of pain and inflammation) and cysteinyl LT receptor antagonists (montelukast and pranlukast for asthma and allergic rhinitis) [ 9 , 11 , 12 ]. PUFA-derived epoxy FAs (EpFAs including EpETrE; LA-derived epoxy-octadecenoic acid, EpOME; ALA-derived epoxy-octadecadienoic acid, EpODE; DHA-derived epoxy-docosapentaenoic acid, EpDPE; and EPA-derived epoxy-eicosatetraenoic acid, EpETE) show anti-inflammatory effects in treating pain, inflammation, cardiovascular diseases, and other conditions [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

A Soluble Epoxide Hydrolase Inhibitor, 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) Urea, Ameliorates Experimental Autoimmune Encephalomyelitis

Jonnalagadda

Wan

Chun

et al. 2021

IJMS

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Polyunsaturated fatty acids (PUFAs) are essential FAs for human health. Cytochrome P450 oxygenates PUFAs to produce anti-inflammatory and pain-resolving epoxy fatty acids (EpFAs) and other oxylipins whose epoxide ring is opened by the soluble epoxide hydrolase (sEH/Ephx2), resulting in the formation of toxic and pro-inflammatory vicinal diols (dihydroxy-FAs). Pharmacological inhibition of sEH is a promising strategy for the treatment of pain, inflammation, cardiovascular diseases, and other conditions. We tested the efficacy of a potent, selective sEH inhibitor, 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU), in an animal model of multiple sclerosis (MS), experimental autoimmune encephalomyelitis (EAE). Prophylactic TPPU treatment significantly ameliorated EAE without affecting circulating white blood cell counts. TPPU accumulated in the spinal cords (SCs), which was correlated with plasma TPPU concentration. Targeted lipidomics in EAE SCs and plasma identified that TPPU blocked production of dihydroxy-FAs efficiently and increased some EpFA species including 12(13)-epoxy-octadecenoic acid (12(13)-EpOME) and 17(18)-epoxy-eicosatrienoic acid (17(18)-EpETE). TPPU did not alter levels of cyclooxygenase (COX-1/2) metabolites, while it increased 12-hydroxyeicosatetraenoic acid (12-HETE) and other 12/15-lipoxygenase metabolites. These analytical results are consistent with sEH inhibitors that reduce neuroinflammation and accelerate anti-inflammatory responses, providing the possibility that sEH inhibitors could be used as a disease modifying therapy, as well as for MS-associated pain relief.

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Fatty acid handling in mammalian cells

Lehner¹,

Quiroga²

2021

Biochemistry of Lipids, Lipoproteins and Membranes

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Targeting Leukotrienes as a Therapeutic Strategy to Prevent Comorbidities Associated with Metabolic Stress

Cited by 3 publications

References 120 publications

Cystic fibrosis management in pediatric population—from clinical features to personalized therapy

Cystic fibrosis management in pediatric population—from clinical features to personalized therapy

A Soluble Epoxide Hydrolase Inhibitor, 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) Urea, Ameliorates Experimental Autoimmune Encephalomyelitis

Fatty acid handling in mammalian cells

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