The Natriuretic Peptide System: A Single Entity, Pleiotropic Effects

Corte, Vittoriano Della; Pacinella, Gaetano; Todaro, Federica; Pecoraro, Rosaria; Tuttolomondo, Antonino

doi:10.3390/ijms24119642

Cited by 8 publications

(1 citation statement)

References 179 publications

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“…Moreover, ANP regulates cardiac morpholog tion, and aging [112,113]. In the pregnant uterus, ANP promotes decidualization a ral artery remodeling in an auto/paracrine mechanism critical for fetal growth [1 paired ANP expression and/or function have been implicated in major cardiovascu eases, including atrial fibrillation, hypertension, cardiac hypertrophy, heart failu pre-eclampsia [111,115].…”

Section: Corin In Pro-anp Processingmentioning

confidence: 99%

Type II Transmembrane Serine Proteases as Modulators in Adipose Tissue Phenotype and Function

Zhang

et al. 2023

Biomedicines

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Adipose tissue is a crucial organ in energy metabolism and thermoregulation. Adipose tissue phenotype is controlled by various signaling mechanisms under pathophysiological conditions. Type II transmembrane serine proteases (TTSPs) are a group of trypsin-like enzymes anchoring on the cell surface. These proteases act in diverse tissues to regulate physiological processes, such as food digestion, salt-water balance, iron metabolism, epithelial integrity, and auditory nerve development. More recently, several members of the TTSP family, namely, hepsin, matriptase-2, and corin, have been shown to play a role in regulating lipid metabolism, adipose tissue phenotype, and thermogenesis, via direct growth factor activation or indirect hormonal mechanisms. In mice, hepsin deficiency increases adipose browning and protects from high-fat diet-induced hyperglycemia, hyperlipidemia, and obesity. Similarly, matriptase-2 deficiency increases fat lipolysis and reduces obesity and hepatic steatosis in high-fat diet-fed mice. In contrast, corin deficiency increases white adipose weights and cell sizes, suppresses adipocyte browning and thermogenic responses, and causes cold intolerance in mice. These findings highlight an important role of TTSPs in modifying cellular phenotype and function in adipose tissue. In this review, we provide a brief description about TTSPs and discuss recent findings regarding the role of hepsin, matriptase-2, and corin in regulating adipose tissue phenotype, energy metabolism, and thermogenic responses.

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Section: Corin In Pro-anp Processingmentioning

confidence: 99%

Type II Transmembrane Serine Proteases as Modulators in Adipose Tissue Phenotype and Function

Zhang

et al. 2023

Biomedicines

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Novel therapeutic perspectives in Noonan syndrome and RASopathies

Saint-Laurent,

Mazeyrie,

Yart

et al. 2023

Eur J Pediatr

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Noonan syndrome belongs to the family of RASopathies, a group of multiple congenital anomaly disorders caused by pathogenic variants in genes encoding components or regulators of the RAS/mitogen-activated protein kinase (MAPK) signalling pathway. Collectively, all these pathogenic variants lead to increased RAS/MAPK activation. The better understanding of the molecular mechanisms underlying the different manifestations of NS and RASopathies has led to the identification of molecular targets for specific pharmacological interventions. Many specific agents (e.g. SHP2 and MEK inhibitors) have already been developed for the treatment of RAS/MAPK-driven malignancies. In addition, other molecules with the property of modulating RAS/MAPK activation are indicated in non-malignant diseases (e.g. C-type natriuretic peptide analogues in achondroplasia or statins in hypercholesterolemia). Conclusion: Drug repositioning of these molecules represents a challenging approach to treat or prevent medical complications associated with RASopathies. What is Known:• Noonan syndrome and related disorders are caused by pathogenic variants in genes encoding components or regulators of the RAS/mitogen-activated protein kinase (MAPK) signalling pathway, resulting in increased activation of this pathway.• This group of disorders is now known as RASopathies and represents one of the largest groups of multiple congenital anomaly diseases known. What is New:• The identification of pathophysiological mechanisms provides new insights into the development of specific therapeutic strategies, in particular treatment aimed at reducing RAS/MAPK hyperactivation.• Drug repositioning of specific agents already developed for the treatment of malignant (e.g. SHP2 and MEK inhibitors) or non-malignant diseases (e.g. C-type natriuretic peptide analogues in achondroplasia or statins in hypercholesterolaemia) represents a challenging approach to the treatment of RASopathies.

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Promising horizons in achondroplasia along with the development of new drugs

Ozono,

Kubota,

Michigami

2024

Endocr J

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Achondroplasia (ACH) is a representative skeletal disorder characterized by rhizomelic shortened limbs and short stature. ACH is classified as belonging to the fibroblast growth factor receptor 3 (FGFR3) group. The downstream signal transduction of FGFR3 consists of STAT1 and RAS/RAF/MEK/ERK pathways. The mutant FGFR3 found in ACH is continuously phosphorylated and activates downstream signals, resulting in abnormal proliferation and differentiation of chondrocytes in the growth plate and cranial base synchondrosis. A patient registry has been developed and has contributed to revealing the natural history of ACH patients. Concerning the short stature, the adult height of ACH patients ranges between 126.7-135.2 cm for men and 119.9-125.5 cm for women in many countries. Along with severe short stature, foramen magnum stenosis and spinal canal stenosis are major complications: the former leads to sleep apnea, breathing disorders, myelopathy, hydrocephalus, and sudden death, and the latter causes pain in the extremities, numbness, muscle weakness, movement disorders, intermittent claudication, and bladder-rectal disorders. Growth hormone treatment is available for ACH only in Japan. However, the effect of the treatment on adult height is not satisfactory. Recently, the neutral endopeptidaseresistant CNP analogue vosoritide has been approved as a new drug for ACH. Additionally in development are a tyrosine kinase inhibitor, a soluble FGFR3, an antibody against FGFR3, meclizine, and the FGF2-aptamer. New drugs will bring a brighter future for patients with ACH.

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The Natriuretic Peptide System: A Single Entity, Pleiotropic Effects

Cited by 8 publications

References 179 publications

Type II Transmembrane Serine Proteases as Modulators in Adipose Tissue Phenotype and Function

Type II Transmembrane Serine Proteases as Modulators in Adipose Tissue Phenotype and Function

Novel therapeutic perspectives in Noonan syndrome and RASopathies

Promising horizons in achondroplasia along with the development of new drugs

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