Nesfatin-1 regulates the phenotype transition of cavernous smooth muscle cells by activating PI3K/AKT/mTOR signaling pathway to improve diabetic erectile dysfunction

Chen, Keming; Huang, Bincheng; Feng, Jiajing; Fan, Shuzhe; Hu, Zhengxing; Ren, Shuai; Tian, Haifu; Abdulkarem, A.L.-QAISIMOHAMMED; Wang, Xuehao; Tuo, Yunshang; Liang, Xiaoxia; Xie, Haibo; He, Rui; Li, Guangyong

doi:10.1016/j.heliyon.2024.e32524

Heliyon

2024

DOI: 10.1016/j.heliyon.2024.e32524

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Nesfatin-1 regulates the phenotype transition of cavernous smooth muscle cells by activating PI3K/AKT/mTOR signaling pathway to improve diabetic erectile dysfunction

Keming Chen,

Bincheng Huang,

Jiajing Feng

et al.

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Cited by 2 publications

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Retraction: Nesfatin-1 regulates the phenotype transition of cavernous smooth muscle cells by activating PI3K/AKT/mTOR signaling pathway to improve diabetic erectile dysfunction

2024

PLoS ONE

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Retraction: Nesfatin-1 regulates the phenotype transition of cavernous smooth muscle cells by activating PI3K/AKT/mTOR signaling pathway to improve diabetic erectile dysfunction

2024

PLoS ONE

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Association between serum NUCB2/nesfatin‑1 levels and erectile dysfunction

Koç,

Gul,

Erkan

et al. 2024

Exp Ther Med

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Erectile dysfunction (ED) is one of the most common complaints in the male sexual health field, with a multifactorial etiology yet to be fully elucidated. Nucleobindin 2 (NUCB2)/nesfatin-1, known for its regulatory role in food intake, can also regulate the vascular, neural and hormonal systems, all of which are of great importance in the etiology of ED. The present study included 43 men with ED and 40 healthy individuals without ED. The participants were assessed using the Turkish version of the International Index of Erectile Function (IIEF-5) to determine the presence and severity of ED. Serum NUCB2/nesfatin-1, total testosterone, fasting blood glucose, hemoglobin A1c, total cholesterol, low-density lipoprotein, high-density lipoprotein, very low-density lipoprotein, triglyceride and total prostate-specific antigen levels were all measured. The mean age of the participants was 46.77±9.87 years with an age range of 25-67 years. The mean ages of the ED and non-ED groups were 47.47±11.19 and 46.03±8.30 years, respectively. Patient age and serum biochemical parameters were found to be comparable between the two groups. The serum NUCB2/nesfatin-1 levels of the ED group were also revealed to be significantly lower compared with those of the non-ED group (P=0.019). There was a weak negative correlation between the serum NUCB2/nesfatin-1 level and the severity of ED according to the IIEF-5 score (r=-0.306; P=0.005). The receiver operating characteristic curve analysis of serum NUCB2/nesfatin-1 revealed a cut-off value of 1.25 ng/ml for distinguishing between the ED and non-ED groups (P=0.019). These findings suggest that reduced serum NUCB2/nesfatin-1 values may be implicated in the etiology of ED. Further studies are required to clarify the effect of NUCB2/nesfatin-1 on vascular physiology and erectile physiology or pathophysiology.

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Nesfatin-1 regulates the phenotype transition of cavernous smooth muscle cells by activating PI3K/AKT/mTOR signaling pathway to improve diabetic erectile dysfunction

Cited by 2 publications

References 27 publications

Retraction: Nesfatin-1 regulates the phenotype transition of cavernous smooth muscle cells by activating PI3K/AKT/mTOR signaling pathway to improve diabetic erectile dysfunction

Retraction: Nesfatin-1 regulates the phenotype transition of cavernous smooth muscle cells by activating PI3K/AKT/mTOR signaling pathway to improve diabetic erectile dysfunction

Association between serum NUCB2/nesfatin‑1 levels and erectile dysfunction

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