Peptides最新文献

{"title":"Peptide‑based therapeutic strategies for glioma: Current state and prospects","authors":"Yajing Mi ,&nbsp;Pengtao Jiang ,&nbsp;Jing Luan ,&nbsp;Lin Feng ,&nbsp;Dian Zhang ,&nbsp;Xingchun Gao","doi":"10.1016/j.peptides.2025.171354","DOIUrl":"10.1016/j.peptides.2025.171354","url":null,"abstract":"<div><div>Glioma is a prevalent form of primary malignant central nervous system tumor, characterized by its cellular invasiveness, rapid growth, and the presence of the blood-brain barrier (BBB)/blood-brain tumor barrier (BBTB). Current therapeutic approaches, such as chemotherapy and radiotherapy, have shown limited efficacy in achieving significant antitumor effects. Therefore, there is an urgent demand for new treatments. Therapeutic peptides represent an innovative class of pharmaceutical agents with lower immunogenicity and toxicity. They are easily modifiable via chemical means and possess deep tissue penetration capabilities which reduce side effects and drug resistance. These unique pharmacokinetic characteristics make peptides a rapidly growing class of new therapeutics that have demonstrated significant progress in glioma treatment. This review outlines the efforts and accomplishments in peptide-based therapeutic strategies for glioma. These therapeutic peptides can be classified into four types based on their anti-tumor function: tumor-homing peptides, inhibitor/antagonist peptides targeting cell surface receptors, interference peptides, and peptide vaccines. Furthermore, we briefly summarize the results from clinical trials of therapeutic peptides in glioma, which shows that peptide-based therapeutic strategies exhibit great potential as multifunctional players in glioma therapy.</div></div>","PeriodicalId":19765,"journal":{"name":"Peptides","volume":"185 ","pages":"Article 171354"},"PeriodicalIF":2.8,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143372529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association among nesfatin-1, obesity category, presence of obesity-related complications, and eating patterns in patients with obesity: Results of a single endocrine centre observational study","authors":"Ewa Milewska-Kobos ,&nbsp;Ewelina Szczepanek- Parulska ,&nbsp;Martyna Marciniak ,&nbsp;Elżbieta Wrotkowska ,&nbsp;Maja Cieślewicz ,&nbsp;Agnieszka Dobrowolska ,&nbsp;Marek Ruchala","doi":"10.1016/j.peptides.2025.171355","DOIUrl":"10.1016/j.peptides.2025.171355","url":null,"abstract":"<div><div>Since its discovery, nesfatin-1 (N1) has been recognised as an anorexigenic agent potentially related to obesity pathogenesis and development, including its modulatory effect on the brain’s reward system and eating behaviours. As the results from human studies examining the relation between N1 serum levels, body mass index (BMI), and metabolic status are scarce and inconclusive, we aimed to investigate the association between serum N1 levels and obesity categories, obesity-related complications, and disturbed eating behaviour. We studied 110 patients with obesity divided into obesity categories according to their BMI and metabolic status. N1 was measured in a fasting state (N1⁰) and 2 h after a glucose load (N1²) and correlated with anthropometric measurements, serum analysis, and the presence of selected obesity-related complications. Neither N1⁰ nor N1² correlated significantly with obesity; however, N1⁰ tended to be high in patients with a high BMI. A positive correlation was observed among N1², fat-free mass (p = 0.022), and muscle mass (p = 0.02). We found positive correlations between N1⁰ and N1² with aspartate aminotransferase (p = 0.012 and p = 0.022, respectively) and alanine aminotransferase (p = 0.027 and p = 0.006, respectively). Patients with dyslipidaemia had significantly higher N1⁰ (p = 0.03) and N1² (p = 0.049) levels. Neither N1⁰ nor N1² correlated significantly with disturbed eating behaviour; however, low N1⁰ levels were associated with a hedonic eating pattern (p = 0.03). N1 may be involved in the pathogenesis of obesity and obesity-related complications; however, owing to the complex mechanisms of its secretion and action, further clinical and experimental research is needed.</div></div>","PeriodicalId":19765,"journal":{"name":"Peptides","volume":"185 ","pages":"Article 171355"},"PeriodicalIF":2.8,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143349232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ghrelin promotes chronic diabetic wound healing by regulating keratinocyte proliferation and migration through the ERK1/2 pathway","authors":"Yukang Zhang ,&nbsp;Yuan Chen ,&nbsp;Kailin Li ,&nbsp;Cong Chen ,&nbsp;Yong Hu ,&nbsp;Xian Li","doi":"10.1016/j.peptides.2025.171350","DOIUrl":"10.1016/j.peptides.2025.171350","url":null,"abstract":"<div><div>Delayed wound healing is a complication of diabetes mellitus and can lead to infection, sepsis, and amputation. Despite the currently available treatments, the global burden of diabetes-related wounds is growing; thus, more effective therapy for diabetic wounds is urgently needed. Ghrelin, an endogenous ligand for the growth hormone secretagogue receptor, is a 28-amino acid peptide hormone. Some reports have confirmed the therapeutic effects of ghrelin on diabetes mellitus and its complications. However, the effects and corresponding mechanisms of ghrelin on chronic diabetic wounds remain unknown. In this study, we explored the effect of ghrelin on diabetic wound healing and investigated the associated mechanisms. We showed that ghrelin accelerated wound healing in diabetic rats by promoting the proliferation and migration of keratinocytes. Re-epithelialization was accelerated in ghrelin-treated wounds, thicker and longer newly formed epidermis and more dividing keratinocytes were observed. We further confirmed that ghrelin regulated keratinocytes by activating the ERK1/2 pathway through its receptor growth hormone secretagogue receptor 1a (GHSR1a). Ghrelin also significantly reduced the levels of pro-inflammatory cytokines and increased the deposition of collagen in diabetic wounds. Our data provides preclinical evidence for the potential application of ghrelin as a compound to promote diabetic wound healing and clarifies the molecular mechanism.</div></div>","PeriodicalId":19765,"journal":{"name":"Peptides","volume":"184 ","pages":"Article 171350"},"PeriodicalIF":2.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of irisin on ovariectomy-induced depression, anxiety, and bodyweight growth in female mice","authors":"Xupei Xie ,&nbsp;Yanling Zhang ,&nbsp;Jianping He","doi":"10.1016/j.peptides.2025.171349","DOIUrl":"10.1016/j.peptides.2025.171349","url":null,"abstract":"<div><div>Hormone replacement therapy (HRT) for postmenopausal syndrome (PMS) carries high risks of undesirable side effects. This study explores irisin as a potential alternative to HRT and investigates the underlying mechanisms. Ovariectomized (OVX) female mice was used as an animal model. The experimental mice were divided into sham, OVX, OVX + irisin (1, 3 μg/kg), OVX+ estradiol (0.5 mg/kg), and OVX + irisin + compound C (AMPK inhibitor) groups. Results showed that OVX induced depression, anxiety, and bodyweight growth in female mice. These OVX-induced abnormalities were reversed by irisin treatment, while AMPK inhibitor abolished irisin’s function, indicating that irisin’s therapeutic effects on OVX mice were achieved by activating AMPK. Moreover, irisin could increase pAMPK levels and ameliorate the overexpression of NF-κB and its downstream factors including inflammatory factors (IL-1β, IL-6, and TNF-α) and neurotoxic mediators (COX-2 and iNOS) in the hippocampus, frontal cortex, and serum of the OVX mice. However, irisin did not affect hypothalamus pAMPK level or food intake. These findings indicate that irisin’s therapeutic effects on depression and anxiety may be linked to its inhibition of inflammatory factors and neurotoxic mediators in the serum and brain, occurring through the AMPK/NF-κB pathway. Additionally, irisin’s effect of reducing bodyweight may be associated with an increase in serum pAMPK level, rather than a direct impact on food intake. Further mechanistic exploration revealed that the beneficial effects of irisin, including both the attenuation of bodyweight gain and the improvement of neurological deficits, are attributed to the activation of αVβ5 receptors.</div></div>","PeriodicalId":19765,"journal":{"name":"Peptides","volume":"184 ","pages":"Article 171349"},"PeriodicalIF":2.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Compensatory mechanisms underlying arginine vasopressin regulation in transient polyuria during pregnancy","authors":"Tetsuro Tsumura ,&nbsp;Daisuke Hagiwara ,&nbsp;Satoshi Naito ,&nbsp;Yuichi Kondo ,&nbsp;Yohei Kawaguchi ,&nbsp;Takashi Miyata ,&nbsp;Tomoko Kobayashi ,&nbsp;Mariko Sugiyama ,&nbsp;Takeshi Onoue ,&nbsp;Shintaro Iwama ,&nbsp;Hidetaka Suga ,&nbsp;Ryoichi Banno ,&nbsp;Hiroshi Arima","doi":"10.1016/j.peptides.2025.171352","DOIUrl":"10.1016/j.peptides.2025.171352","url":null,"abstract":"<div><div>Transient polyuria during pregnancy is reportedly caused by increased arginine vasopressin (AVP) degradation due to vasopressinase produced by the placenta. The mechanism underlying transient polyuria during pregnancy has not been established. In this study we measured urine volume, urine osmolality, and AVP transcriptional activity during pregnancy in wild-type and familial neurohypophysial diabetes insipidus (FNDI) mice. The FNDI mice were used as a partial AVP deficiency model. Vasopressinase was shown to be present in the placentas of pregnant mice. The <em>Avp</em> hnRNA level in the supraoptic nucleus, which is indicative of AVP transcriptional activity, was upregulated in wild-type and FNDI mice during late pregnancy. FNDI mice, but not wild-type mice, had a significant increase in urine volume and a decrease in urine osmolality during pregnancy. These data suggest that an increase in urine volume during pregnancy only occurs when the compensatory increase in AVP release is insufficient to counteract degradation by vasopressinase.</div></div>","PeriodicalId":19765,"journal":{"name":"Peptides","volume":"184 ","pages":"Article 171352"},"PeriodicalIF":2.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143053122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phoenixin's influence on HPG axis and inflammation in elite ice hockey athletes: A cross-sectional analysis","authors":"Liang Fang ,&nbsp;Yixing Chang ,&nbsp;Qiuyan Liang ,&nbsp;Ruiqi Huang ,&nbsp;Xuejie Yi ,&nbsp;Tingting Yao","doi":"10.1016/j.peptides.2025.171351","DOIUrl":"10.1016/j.peptides.2025.171351","url":null,"abstract":"<div><div>The neuropeptide phoenixin (PNX) may be involved in regulating the hypothalamic-pituitary-gonadal (HPG) axis and inflammatory responses. This study aims to investigate the role of PNX in the regulation of HPG axis function in ice hockey players and its impact on body composition. This cross-sectional study included 65 male ice hockey players aged 18–22, divided into untrained, non-elite athlete, and elite athlete groups. Body composition was assessed using bioelectrical impedance analysis, and plasma levels of PNX, gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH), testosterone, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10) were measured by enzyme-linked immunosorbent assay. Elite ice hockey players exhibited significantly higher lower limb and core skeletal muscle mass, skeletal muscle index, and testosterone levels, aligning with the high-intensity intermittent nature of hockey training. Compared to the non-training group, ice hockey training groups showed elevated levels of PNX, GnRH, testosterone, and TNF-α, along with reduced levels of LH and IL-6. PNX concentration positively correlated with lean body mass, skeletal muscle mass, skeletal muscle index, serum GnRH, and testosterone levels, and negatively correlated with serum LH and IL-6 levels. In conclusion, PNX may enhance skeletal muscle mass in ice hockey players, particularly in the lower limbs and core muscles, by promoting HPG axis activity while inhibiting inflammatory responses and reducing HPG axis suppression. These findings provide new insights into the physiological adaptation mechanisms of ice hockey players, potentially aiding in the optimization of training strategies and improvement of athletic performance.</div></div>","PeriodicalId":19765,"journal":{"name":"Peptides","volume":"184 ","pages":"Article 171351"},"PeriodicalIF":2.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcardiac gradients of pro-cholecystokinin, cholecystokinin, and gastrin in patients with and without heart failure with reduced ejection fraction","authors":"Tania Deis ,&nbsp;Benedicte Heegaard ,&nbsp;Kasper Rossing ,&nbsp;Berit Philbert ,&nbsp;Michael Vinther ,&nbsp;Niels Risum ,&nbsp;Peter Karl Jacobsen ,&nbsp;Jens P. Goetze ,&nbsp;Finn Gustafsson","doi":"10.1016/j.peptides.2025.171353","DOIUrl":"10.1016/j.peptides.2025.171353","url":null,"abstract":"<div><h3>Background</h3><div>Cholecystokinin (CCK) is secreted from the intestines in response to food intake. We previously reported that the CCK gene is also expressed in the mammalian heart, and it has been hypothesized that proCCK could be a novel cardiac biomarker. However, it is not known whether cardiac gene expression leads to secretion in humans.</div></div><div><h3>Purpose</h3><div>To investigate myocardial secretion of proCCK in patients with heart failure with reduced ejection fraction (HFrEF) or arrythmias.</div></div><div><h3>Methods</h3><div>A total of 115 patients undergoing invasive cardiac procedures were included: 55 with HFrEF (67 years [interquartile range (IQR) 60–76], 72.7 % male, LVEF 30 % [IQR 20–35]), and 60 without HFrEF (26 with Wolff-Parkinson-White syndrome (WPW) (30 years [IQR 26–39], 61.5 % male), and 34 with atrial fibrillation (AFIB) (66 years [IQR 60–71], 61.8 % male)). Blood was collected from the coronary sinus (CS) as well as the left atrium or femoral artery (A) to determine the transcardiac concentration gradient (TC_proCCK) (CS proCCK concentration - A proCCK concentration). Radioimmunoassays were used for measurements of plasma hormones.</div></div><div><h3>Results</h3><div>TC_proCCK across failing hearts was 0.05 pmol/l (IQR: −1.49–2.67) (<em>p = 0.365</em>). In non-failing hearts, TC_proCCK was 0.35 pmol/l (IQR: −1.57–1.29) (<em>p = 0.778</em>) for WPW and 0.68 pmol/l (IQR: −1.58–3.28) (<em>p = 0.133</em>) for AFIB. Transcardiac gradients for N-terminal pro B-type natriuretic peptide (NT-proBNP) were observed in all groups.</div></div><div><h3>Conclusions</h3><div>No evidence of net myocardial secretion of proCCK was found in either failing or structurally normal hearts, questioning its proposed role as a cardiac biomarker.</div></div>","PeriodicalId":19765,"journal":{"name":"Peptides","volume":"184 ","pages":"Article 171353"},"PeriodicalIF":2.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143060018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apelin/APJ increased renal blood flow through endothelial BKCa channel induced p-eNOS and ET-1 in diabetic conditions","authors":"Mingcong Huang ,&nbsp;Jing Chang ,&nbsp;Yu Liu ,&nbsp;Jiming Yin ,&nbsp;Xiangjun Zeng","doi":"10.1016/j.peptides.2024.171333","DOIUrl":"10.1016/j.peptides.2024.171333","url":null,"abstract":"<div><div>Renal hemodynamics damage, an important driving mechanism of diabetic nephropathy (DN), is related to many abnormal endothelial released molecules, such as endothelial nitrogen monoxide synthase (eNOS) and endothelin-1 (ET-1), caused by glomerular endothelial cells dysfunction. Apelin, as the endogenous ligand for APJ, was reported to be associated with endothelial cell dysfunction in diabetes. Therefore, it is hypothesized that apelin/APJ increased renal perfusion in DN through regulating endothelial released molecules. Diabetic models were replicated via injecting STZ intraperitoneally (40 mg/kg/day) for 5 consecutive days. Apelin-13 was infused with micro-osmotic pump at 30 μg/kg/day for 4 weeks. The results showed that apelin increased renal blood flow by increasing phosphorylated eNOS and decreasing ET-1 in diabetic mice, which were cancelled in endothelial-specific APJ knockout mice or whole-body large conductance Ca^2 +-activated K⁺ (BKCa) channel knockout rats. Additionally, apelin/APJ activated BKCa channel via increasing expression of BKCa subunits through PI3K/AKT/GSK-3β/Nrf2 pathway but not increasing intracellular Ca²⁺ concentration under high glucose conditions. In conclusion, this study revealed that apelin/APJ increased renal blood flow in early phase of DN via increasing p-eNOS and decreasing ET-1 in glomerular endothelial cells dependent on PI3K/AKT/GSK-3β/Nrf2 pathway induced expression of BKCa subunits.</div></div>","PeriodicalId":19765,"journal":{"name":"Peptides","volume":"183 ","pages":"Article 171333"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Octadecaneuropeptide promotes the migration of astrocyte via ODN metabotropic receptor and calcium signaling pathway","authors":"Sada Al-Mashhadani ,&nbsp;Mariem Sallemi ,&nbsp;Amira Namsi ,&nbsp;Yosra Hamdi ,&nbsp;Amine Cherif ,&nbsp;Fethia Abidi ,&nbsp;Jérôme Leprince ,&nbsp;Zekri Sami ,&nbsp;David Vaudry ,&nbsp;Masmoudi-Kouki Olfa","doi":"10.1016/j.peptides.2024.171338","DOIUrl":"10.1016/j.peptides.2024.171338","url":null,"abstract":"<div><div>Migration is an essential characteristic of cells that occurs during many physiological and pathological processes. Astrocytes represent the most abundant cell type in the adult central nervous system (CNS), that play a crucial role in various functions such as guiding and supporting neuronal migration during development and maintaining brain homeostasis at adulthood. Astrocytes specifically synthesize and release endozepines, a family of regulatory peptides, including the octadecaneuropeptide (ODN). ODN is an endogenous ligand for both central-type benzodiazepine receptors and a metabotropic receptor. ODN promotes proliferation and prevents oxidative damage induced apoptosis on both neurons and astrocytes. However, little is known regarding the effect of ODN on cell migration. The purpose of the present study was to investigate the potential effect of ODN on astrocytes migration. Our results show that ODN stimulates astrocytes proliferation and migration at very low concentrations in wound healing assays, that was mimicked by the metabotropic ODN receptor agonist cyclo_1–8 octapeptide (cyclo_1–8OP, 10⁻¹⁴ M to 10⁻¹⁰ M). The effect of ODN on astrocyte migration was abrogated by the metabotropic receptor antagonist, cyclo_1–8[DLeu⁵] OP. Moreover, we have shown that ODN activates the calcium signaling pathway and increases the <em>mammalian target of rapamycin (mTOR)</em> gene transcription, which are both known to promote astrocyte migration. Therefore, the present results suggest that ODN regulates astroglial cell migration through the calcium/mTOR signaling pathway and provide new insight regarding the role of ODN on brain remodling after injury.</div></div>","PeriodicalId":19765,"journal":{"name":"Peptides","volume":"183 ","pages":"Article 171338"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated Plasma Soluble (Pro)renin receptor as a potential indicator for heart failure","authors":"Jianhua Xiong ,&nbsp;Huiru Yang ,&nbsp;Xiaoli Yi ,&nbsp;Xu Zhou ,&nbsp;Wenting Tan ,&nbsp;Shanshan Song ,&nbsp;Chunju Liu ,&nbsp;Mulan Wang ,&nbsp;Mengzhi Zhu ,&nbsp;Lixiang Zheng ,&nbsp;Jun Yu ,&nbsp;Chuanming Xu","doi":"10.1016/j.peptides.2024.171337","DOIUrl":"10.1016/j.peptides.2024.171337","url":null,"abstract":"<div><div>Increasing evidence has demonstrated that sPRR [a truncated soluble form of (pro)renin receptor] levels may reflect the severity of several diseases, including kidney disease, hypertension, and heart failure (HF). Although previous studies using cohorts primarily consisting of HF patients with reduced ejection fraction revealed that increased plasma sPRR levels may be a promising evaluative indicator for HF, definitive information on the relationship between plasma sPRR levels and HF patients with preserved ejection fraction (HFpEF) is still insufficient and scarce. In the present study, we further clarified the status of plasma sPRR levels in HF patients by meta-analysis. We enrolled a cohort primarily consisting of HFpEF patients (87.8 %) to further determine the relationships between plasma sPRR levels and HFpEF. Meta-analysis showed a significant increase in plasma sPRR levels in HF patients, with substantial statistical heterogeneity. In our observational study, plasma sPRR levels were significantly higher in the HF group than in the non-HF group (17.4 ± 9.8 vs. 10.4 ± 3.4 ng/ml, p &lt; 0.001) and positively correlated with age, B-type natriuretic peptide, creatine, urea nitrogen, plasma renin activity, angiotensin II, and left atrial diameter and negatively correlated with estimated glomerular filtration rate. Plasma sPRR levels (The average value ≥ 16.1 ± 7.2 ng/ml) and the diagnostic values (reflected by the area under the receiver operating characteristic curves ≥ 0.749) of sPRR were comparable for all subtypes of HF patients. Overall, plasma sPRR levels were significantly elevated in HF patients. Elevated plasma sPRR levels may be one of the underlying indicators for HF.</div></div>","PeriodicalId":19765,"journal":{"name":"Peptides","volume":"183 ","pages":"Article 171337"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}