Interventions in the <scp>B</scp>‐type natriuretic peptide signalling pathway as a means of controlling chronic itch

Meng, Jianghui; Chen, Weiwei; Wang, Jiafu

doi:10.1111/bph.14952

Cited by 21 publications

(17 citation statements)

References 152 publications

(234 reference statements)

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“…This involves IL-31 and itch-selective neuropeptide B-type natriuretic peptide (BNP) ( 9 ). First, IL-31 upregulates itch-related neuropeptide BNP synthesis and induces its release from mouse sensory neurons ( 6 , 128 ) ( Figure 1D ). Second, BNP binds to its receptor NPR1 located on human keratinocytes and induces upregulation of TRPV3 transcriptional levels ( 9 ) ( Figure 1D ).…”

Section: Mechanisms For Th2-promoted Trp Channel Sensitizationmentioning

confidence: 99%

Th2 Modulation of Transient Receptor Potential Channels: An Unmet Therapeutic Intervention for Atopic Dermatitis

Meng

Fischer

et al. 2021

Front. Immunol.

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Atopic dermatitis (AD) is a multifaceted, chronic relapsing inflammatory skin disease that affects people of all ages. It is characterized by chronic eczema, constant pruritus, and severe discomfort. AD often progresses from mild annoyance to intractable pruritic inflammatory lesions associated with exacerbated skin sensitivity. The T helper-2 (Th2) response is mainly linked to the acute and subacute phase, whereas Th1 response has been associated in addition with the chronic phase. IL-17, IL-22, TSLP, and IL-31 also play a role in AD. Transient receptor potential (TRP) cation channels play a significant role in neuroinflammation, itch and pain, indicating neuroimmune circuits in AD. However, the Th2-driven cutaneous sensitization of TRP channels is underappreciated. Emerging findings suggest that critical Th2-related cytokines cause potentiation of TRP channels, thereby exaggerating inflammation and itch sensation. Evidence involves the following: (i) IL-13 enhances TRPV1 and TRPA1 transcription levels; (ii) IL-31 sensitizes TRPV1 via transcriptional and channel modulation, and indirectly modulates TRPV3 in keratinocytes; (iii) The Th2-cytokine TSLP increases TRPA1 synthesis in sensory neurons. These changes could be further enhanced by other Th2 cytokines, including IL-4, IL-25, and IL-33, which are inducers for IL-13, IL-31, or TSLP in skin. Taken together, this review highlights that Th2 cytokines potentiate TRP channels through diverse mechanisms under different inflammatory and pruritic conditions, and link this effect to distinct signaling cascades in AD. This review strengthens the notion that interrupting Th2-driven modulation of TRP channels will inhibit transition from acute to chronic AD, thereby aiding the development of effective therapeutics and treatment optimization.

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Section: Mechanisms For Th2-promoted Trp Channel Sensitizationmentioning

confidence: 99%

Th2 Modulation of Transient Receptor Potential Channels: An Unmet Therapeutic Intervention for Atopic Dermatitis

Meng

Fischer

et al. 2021

Front. Immunol.

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“…Structurally, it is similar to the GC-A, but predominantly localized in bone and ovary tissue make the key actions in stimulation of endochondral ossification required for long bone growth and oocyte maturation. Because of its localization in the cardiovascular system, smooth muscle cells and fibroblasts GC-B seem to be one of the most important mGCs in heart failure [ 18 , 22 , 23 , 24 , 25 , 26 , 27 , 28 ]. GC type C is activated by different peptide agonists: guanylin and uroguanylin.…”

Section: Guanylate Cyclasesmentioning

confidence: 99%

Current Modulation of Guanylate Cyclase Pathway Activity—Mechanism and Clinical Implications

Grześk

Nowaczyk

2021

Molecules

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For years, guanylate cyclase seemed to be homogenic and tissue nonspecific enzyme; however, in the last few years, in light of preclinical and clinical trials, it became an interesting target for pharmacological intervention. There are several possible options leading to an increase in cyclic guanosine monophosphate concentrations. The first one is related to the uses of analogues of natriuretic peptides. The second is related to increasing levels of natriuretic peptides by the inhibition of degradation. The third leads to an increase in cyclic guanosine monophosphate concentration by the inhibition of its degradation by the inhibition of phosphodiesterase type 5. The last option involves increasing the concentration of cyclic guanosine monophosphate by the additional direct activation of soluble guanylate cyclase. Treatment based on the modulation of guanylate cyclase function is one of the most promising technologies in pharmacology. Pharmacological intervention is stable, effective and safe. Especially interesting is the role of stimulators and activators of soluble guanylate cyclase, which are able to increase the enzymatic activity to generate cyclic guanosine monophosphate independently of nitric oxide. Moreover, most of these agents are effective in chronic treatment in heart failure patients and pulmonary hypertension, and have potential to be a first line option.

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“…118 BNP was also detected in the epidermis of the lesion area in AD, indicating that BNP may play an itching-promoting role both in the spinal cord and skin. 119 In addition, BNP can cause keratinocytes to secrete several inflammatory regulators through the GSK3 pathway, such as IL-17A, CXCL10 or MMP9. 120 IL-31, as an itch-promoting factor in AD, can up-regulate the contents of BNP in dorsal root ganglion neurons and skin, causing the synergistic itch.…”

Section: Brain Natriuretic Peptide (Bnp)mentioning

confidence: 99%

Current views on neuropeptides in atopic dermatitis

Zhang

Jiang

et al. 2021

Experimental Dermatology

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Atopic dermatitis (AD) is a chronic inflammatory skin disease involving skin barrier dysfunction and immune imbalance. However, the mechanism of AD is not clear completely and may be related to heredity and environment. Neuropeptides are a class of peptides secreted by nerve endings, they may play roles in promoting vasodilation, plasma extravasation, chemotaxis of inflammatory cells and mediating pruritus. Since itching and immune cell infiltration are the main manifestations of atopic dermatitis, to further investigate the impact of neuropeptides on AD, our review summarized the mechanisms of several common neuropeptides in AD and hypothesized that neuropeptides may be the novel potential targets in AD treatment.

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Interventions in the B‐type natriuretic peptide signalling pathway as a means of controlling chronic itch

Cited by 21 publications

References 152 publications

Th2 Modulation of Transient Receptor Potential Channels: An Unmet Therapeutic Intervention for Atopic Dermatitis

Th2 Modulation of Transient Receptor Potential Channels: An Unmet Therapeutic Intervention for Atopic Dermatitis

Current Modulation of Guanylate Cyclase Pathway Activity—Mechanism and Clinical Implications

Current views on neuropeptides in atopic dermatitis

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