C-type natriuretic peptide and its contribution to bone growth

Kulik-Rechberger, Beata; Trojanowska-Szostek, Maria

doi:10.26444/aaem/140076

Cited by 1 publication

(1 citation statement)

References 40 publications

(59 reference statements)

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“…CNP is now regarded as an autocrine/paracrine regulator with broad expression in the body [ 23 ]. CNP produces a series of biological effects by the cGMP signaling pathway through binding to its specific natriuretic peptide receptor B (NPR-B) [ 24 , 25 ], such as regulation of the proliferation of myocardial cells [ 26 ]; maintaining cardiovascular homeostasis [ 27 ]; inhibition of bone growth and cartilage development [ 28 ]; promote follicular development [ 29 ]. Our group’s previous studies have already shown that CNP can induce sperm capacitation in normal people through cGMP [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

C-Type Natriuretic Peptide (CNP) Could Improve Sperm Motility and Reproductive Function of Asthenozoospermia

Dong

et al. 2022

IJMS

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This study is to analyze the effect of C-type natriuretic peptide (CNP) on sperm motility of asthenozoospermia and explore the influence mechanism of CNP on the reproductive system and sperm motility. Our results showed that the concentration of CNP in asthenospermia patients’ semen was lower than in normal people’s. The motility of sperm could be improved markedly by CNP and 8-Br-cGMP, while the effect of CNP was inhibited by NPR-B antagonist and KT5823. In the asthenozoospermia mouse model induced by CTX, CNP injection could improve sperm motility in the epididymis, alleviate tissue damage in the testes and epididymis, and increase testosterone levels. The asthenospermia mouse model showed high activity of MDA and proinflammatory factors (TNF-α, IL-6), as well as low expression of antioxidants (SOD, GSH-Px, CAT) in the testis and epididymis, but this situation could be significantly ameliorated after being treated with CNP. Those studies indicated that the concentration of CNP in the semen of asthenospermia patients is lower than in normal people and could significantly promote sperm motility through the NPR-B/cGMP pathway. In the asthenospermia mouse model induced by CTX, CNP can alleviate the damage of cyclophosphamide to the reproductive system and sperm motility. The mechanism may involve increasing testosterone and reducing ROS and proinflammatory factors to damage the tissue and sperm.

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