Neuropeptides最新文献

{"title":"Role of interplay between endocannabinoids and neuropeptides in pathogenesis and therapy of depressive and anxiety disorders.","authors":"Miłosz Gołyszny, Jonasz Dragon, Ewa Obuchowicz","doi":"10.1016/j.npep.2025.102564","DOIUrl":"https://doi.org/10.1016/j.npep.2025.102564","url":null,"abstract":"<p><p>A growing body of evidence suggests the existence of a neurochemical and functional interplay between endocannabinoids and neuropeptides, which are both relevant for the pathomechanism and effects of pharmacotherapy in depressive and anxiety disorders. Here, we review the available data on how endocannabinoids influence the activity of the neuropeptidergic systems and conversely, how neuropeptides affect the endocannabinoid system. The explicit/implicit interactions in the relationship of endocannabinoids-neuropeptides are presented. Our paper focuses on both well-known neuropeptides, i.e., corticotropin-releasing hormone/factor, CRH/CRF; oxytocin, OT; arginine-vasopressin, AVP; neuropeptide Y, NPY; orexins/hypocretins, OXs/HCRTs) and less investigated neuropeptides, i.e., nesfatin-1, NEFA; phoenixin, PNX; spexin, SPX; neuropeptide S, NPS). Of all of the brain regions that have been studied, the direct and indirect bidirectional interactions between endocannabinoids and the neuropeptides has most clearly been established in the hypothalamus. It has been proven that neuropeptides are modulators of the multifaceted effects of the endocannabinoid system, namely, its influence on neuroendocrine (CRH/CRF) and behavioral stress responsivity (CRH/CRF, OXs), sociability (OT), feelings of pleasure (OXs/HCRTs, NPS), appetite control (NPY, OXs/HCRTs, CRH/CRF, NEFA) and nociception (OT). This latter effect has only the desirable support of positive influence of endocannabinoids on emotional homeostasis to some extent. Nowadays, increasing attention is being paid to the interplay between endocannabinoids and the less explored peptides, especially NEFA and NPS. This trend is both desirable and necessary for gaining a better understanding of the neurochemical aspects and for providing new insights into the potential therapeutic implications in the treatment of affective disorders.</p>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"114 ","pages":"102564"},"PeriodicalIF":2.7,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145308649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory modulation of gastrointestinal motility in mice by Tyr-c[D-Lys-Gly-p-F-Phe-Asp]-D-Pro-NH2, a novel cyclic hexapeptide with multifunctional opioid agonism","authors":"Weifan Ding,&nbsp;Qinqin Zhang,&nbsp;Mengna Zhang,&nbsp;Ning Li,&nbsp;Biao Xu,&nbsp;Yaqi Song,&nbsp;Quan Fang,&nbsp;Nan Zhang","doi":"10.1016/j.npep.2025.102565","DOIUrl":"10.1016/j.npep.2025.102565","url":null,"abstract":"<div><div>Opioid analgesics are critical for managing moderate-to-severe pain，yet are limited by adverse gastrointestinal (GI) effects, notably constipation. This necessitates developing novel opioid agonists with robust analgesia and reduced GI side effects. The cyclic hexapeptide Tyr-c[<em>D</em>-Lys-Gly-<em>p</em>-F-Phe-Asp]-<em>D</em>-Pro-NH₂ (analog 15), a recently characterized multifunctional agonist of μ-opioid receptor (MOR), κ-opioid receptor (KOR), and δ-opioid receptor (DOR), exhibits potent antinociception following subcutaneous (s.c.) administration with constipation observed only at high doses. To further evaluate its GI impact, we assessed the effects of analog 15 on intestinal motility using in vivo upper GI transit and colonic bead expulsion assays. Our results indicated that fentanyl, analog 15, and its parent peptide analog 0 dose-dependently slowed upper GI transit and colonic expulsion after s.c. administration, with the upper GI tract exhibiting greater sensitivity. Mechanistically, fentanyl inhibited the GI motility via both central and peripheral opioid receptors, whereas analog 15 inhibited upper GI transit exclusively through the peripheral MOR, KOR, and DOR, and suppressed colonic transit via the peripheral MOR and KOR, both effects were independent of the central opioid receptor pathway. In conclusion, we demonstrated that the high doses of analog 15 inhibited GI motility through peripherally restricted activation of multiple opioid receptors. This finding aligns with analog 15's limited blood-brain barrier (BBB) permeability, which explains its reduced constipating effects while preserving potent analgesia, thereby supporting the therapeutic potential of multi-target peripheral opioid agonists.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"114 ","pages":"Article 102565"},"PeriodicalIF":2.7,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145267862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of neuropathological pathways by bioactive peptides and proteins/polypeptides: Targeting oxidative stress in neurodegenerative diseases","authors":"Sushil Giri,&nbsp;Phool Chandra","doi":"10.1016/j.npep.2025.102563","DOIUrl":"10.1016/j.npep.2025.102563","url":null,"abstract":"<div><div>Neurodegenerative disorders (NDDs) pose a growing global health burden, primarily due to their progressive nature and the limited efficacy of existing treatments. Bioactive peptides and proteins/polypeptides, particularly those derived from dietary and natural sources, show promise in modulating neurobiological pathways central to neurodegeneration. This review aims to critically examine the neuroprotective roles of Bioactive peptides and proteins/polypeptides in NDDs, elucidating their mechanisms of action, potential therapeutic applications in conditions like Alzheimer's, Parkinso's disease, Huntington's disease, and others, as well as the trends in peptide-based therapeutics. Bioactive peptides and proteins/polyspeptides, such as NGF, BDNF, GDNF, Semax, and Exendin-4, have been found to modulate several critical mechanisms, including the reduction of oxidative stress (OS), inhibition of neuroinflammation, preservation of mitochondria, and enhancement of synaptic plasticity. These peptides have demonstrated efficacy in preclinical and early-phase clinical trials across a spectrum of NDDs. Delivery challenges, such as blood-brain barrier (BBB) permeability and enzymatic degradation, have been acknowledged. Ongoing innovations in peptide engineering, nanoparticle-based delivery systems, CRISPR-assisted design, and AI-driven screening are addressing these limitations. By targeting multiple pathogenic mechanisms simultaneously, peptide-based therapeutics present a rational and innovative approach to NDD management. Their multifunctional action profiles and ability to target specific molecular pathways highlight their potential as next-generation neuroprotective agents. However, future clinical validation and advanced strategies are essential for translating these promising molecules into effective treatments.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"114 ","pages":"Article 102563"},"PeriodicalIF":2.7,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145155841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kisspeptin-54 ameliorates chondrocyte senescence in osteoarthritis via SIRT3-mediated telomere protection and p53 acetylation inhibition","authors":"Zhuobin Yang,&nbsp;Jimo Li,&nbsp;Wenfeng Jin,&nbsp;Dongfeng Cai,&nbsp;Jing Zhang,&nbsp;Song Hong","doi":"10.1016/j.npep.2025.102562","DOIUrl":"10.1016/j.npep.2025.102562","url":null,"abstract":"<div><h3>Background</h3><div>Osteoarthritis (OA), characterized by chondrocyte senescence and oxidative stress, affects over 300 million people globally. Kisspeptin-54, a neuropeptide with pleiotropic protective effects, was investigated for its role in chondrocyte senescence and its underlying mechanisms.</div></div><div><h3>Methods</h3><div>Oxidative stress and senescence were induced in primary mouse chondrocytes by treating them with TBHP. Kisspeptin-54 was administered at varying concentrations (10–1000 nM) to assess cytoprotection, while SIRT3 was knocked down using adenoviral shRNA to validate mechanistic pathways. Telomere length, mTERT expression, telomerase activity, and p53 acetylation were evaluated via Southern blot, RT-PCR, and western blot techniques. Furthermore, senescence was evaluated through the application of SA-β-galactosidase staining alongside the measurement of PAI-1 expression.</div></div><div><h3>Results</h3><div>TBHP induced dose-dependent GPR54 downregulation, oxidative stress (260 % increase in ROS), telomere attrition (41 % reduction in length), and senescence (270 % increase in SA-β-galactosidase-positive cells). Kisspeptin-54 (≤200 nM) rescued cell viability, reduced LDH release (57 % at 200 nM), and mitigated ROS and SOD activity decline. Mechanistically, Kisspeptin-54 restored SIRT3 expression, suppressed p53 acetylation (Acetyl-p53[K382] reduced by 56 % at 200 nM), and preserved telomere function (telomere length restored to 91 % of control). SIRT3 knockdown abrogated these effects, confirming its critical role.</div></div><div><h3>Conclusion</h3><div>Kisspeptin-54 alleviates chondrocyte senescence via a dual mechanism: (1) SIRT3-mediated restoration of mitochondrial antioxidant capacity and telomere homeostasis; (2) inhibition of p53 hyperacetylation and downstream senescence signaling. These findings establish Kisspeptin-54 as an innovative therapeutic candidate for OA acting through the modulation of the SIRT3/p53 axis to combat oxidative stress and telomere dysfunction.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"114 ","pages":"Article 102562"},"PeriodicalIF":2.7,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145192092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nesfatin1 attenuates autism-like behavior via antioxidant, anti-inflammatory activities in a prenatal valproic acid-induced rat model of autism","authors":"Mitra Farbin ,&nbsp;Razieh Hajisoltani ,&nbsp;Tourandokht Baluchnejadmojarad ,&nbsp;Anahita Hejazi ,&nbsp;Touqeer Ahmed ,&nbsp;Heshmatollah Parsian ,&nbsp;Soraya Mehrabi","doi":"10.1016/j.npep.2025.102561","DOIUrl":"10.1016/j.npep.2025.102561","url":null,"abstract":"<div><div>Nesfatin1, a multifunctional peptide involved in energy homeostasis and neural regulation, has emerged as a promising candidate for modulating neurodevelopmental disorders. The anti-inflammatory, antioxidant, and neuroprotective properties of Nesfatin1 have been proven in the central nervous system (CNS). Therefore, it has emerged as a candidate for targeted therapy of various neurological condition. Autism Spectrum Disorder (ASD) is a significant neurological disorder. Considering the importance of these mechanisms demonstrated by Nefastine1, The current study aimed to investigate the therapeutic potential and mechanisms of Nesfatin1 in a rat model of autism. This study evaluated the therapeutic potential of Nesfatin1 in a rodent model of autism induced by prenatal exposure to valproic acid (VPA). Pregnant Wistar rats received VPA on embryonic day 12.5, and male offspring were subsequently assessed for autism-like behaviors using a comprehensive battery of tests, including the three-chamber social interaction test, marble burying, shuttle box passive avoidance, and the elevated plus maze. Following behavioral testing, rats were euthanized, and blood samples were collected via transcardial perfusion. Serum oxytocin levels were measured, and hippocampal tissues were analyzed for inflammatory markers (IL-6, TNF-α) using ELISA. Additionally, total antioxidant capacity (TAC) and the activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD) were assessed. VPA-exposed rats exhibited significant social deficits, increased repetitive behaviors, and impaired cognitive performance, accompanied by heightened neuroinflammation and oxidative stress. Notably, treatment with Nesfatin1 markedly improved social engagement and preference, reduced anxiety and repetitive behaviors, and restored biochemical parameters toward normal levels. Results showed that possible therapeutic mechanism of Nefastin1 are by decreasing inflammation and reducing markers of oxidative stress, while concurrently elevating levels of oxytocin, in addition to the other unknown mechanisms.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"114 ","pages":"Article 102561"},"PeriodicalIF":2.7,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145109618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic potential of small peptides in Alzheimer's disease: Advances in memory restoration and targeted delivery systems","authors":"Poonam Verma ,&nbsp;Rubina Khatun ,&nbsp;Kiran Anjum Jew ,&nbsp;Shakti Ketan Prusty ,&nbsp;Shira Knafo","doi":"10.1016/j.npep.2025.102559","DOIUrl":"10.1016/j.npep.2025.102559","url":null,"abstract":"<div><div>Despite extensive research into Alzheimer's disease (AD), few therapeutic strategies have successfully addressed its core pathology at the synaptic level. Small peptides represent a promising class of therapeutic agents capable of modulating key molecular pathways involved in amyloid toxicity, tau hyperphosphorylation, and synaptic degeneration. Their unique ability to cross biological barriers, interact with intracellular targets, and be modified for enhanced stability positions them as viable candidates for next-generation treatments targeting cognitive decline in AD.Small peptides show strong therapeutic potential yet face challenges in clinical application due to poor bioavailability and rapid enzymatic degradation. To deal with these limitations, various delivery strategies such as intranasal administration, nanoparticle encapsulation, and chemical modification have been developed. When combined with advanced delivery systems, small peptides hold significant promise for mitigating synaptic dysfunction and slowing the progression of Alzheimer's disease. In this review, we examine the mechanisms of action of four small peptides that demonstrate potential in alleviating Alzheimer's-related symptoms. We also evaluate the most effective delivery methods, emphasizing how these approaches enhance the peptides' therapeutic efficacy.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"114 ","pages":"Article 102559"},"PeriodicalIF":2.7,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145007744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of salivary neurotensin and oxytocin in emotional responses to stress inoculation","authors":"Matthew Branney ,&nbsp;Madison Propp ,&nbsp;Dalton Jensen ,&nbsp;Anoushka Singh ,&nbsp;Mark Payton ,&nbsp;Rebecca Ryznar","doi":"10.1016/j.npep.2025.102560","DOIUrl":"10.1016/j.npep.2025.102560","url":null,"abstract":"<div><div>Neuropeptides comprise a class of signaling molecules that exert direct effects on target tissues and modulatory influences across multiple physiological systems; however, their roles in mediating stress responses remains incompletely characterized. Previous studies have shown that acute stress alters salivary levels of neuropeptides but the extent to which these alterations are associated with mechanisms of stress inoculation and emotional valence requires exploration. This study aimed to examine the relationship between salivary neuropeptides and emotional valence following acute stress in military medical students. Salivary samples for oxytocin, neurotensin and data from two questionnaires, ACE and SPANE, were collected from participants pre- and post-stress inoculation. Spearman rank correlation analysis revealed positive correlations &gt;0.9 for neurotensin and oxytocin at pre- and post-inoculation. Post-inoculation neurotensin showed an inverse correlation with pre-simulation SPANE-P and SPANE-B scores (<em>p</em> = 0.006 and <em>p</em> = 0.009 respectively) and demonstrated a positive correlation with pre-simulation SPANE-N score (<em>p</em> = 0.043). Post-inoculation oxytocin demonstrated a negative correlation with pre-inoculation SPANE-P and SPANE-B scores (<em>p</em> = 0.007 and p = 0.006 respectively). Cohorts were established of participants whose neuropeptide levels increased or decreased during inoculation. Inverse correlations existed between oxytocin post-simulation and post-SPANE positive emotions in the increased oxytocin group (<em>R</em> = −0.4607), and between pre-simulation oxytocin and pre-SPANE positive emotions in the decreased oxytocin group (<em>R</em> = −0.4005). Individual variability in salivary neuropeptide responses to inoculation was inversely associated with positive affect, suggesting these neuropeptides as modulators of affective stress responsivity. Future studies should explore the mechanism of these associations and evaluate the potential of salivary neuropeptides as biomarkers for emotional and stress adaptation.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"114 ","pages":"Article 102560"},"PeriodicalIF":2.7,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145047495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Substance P mitigates lipopolysaccharide induced cognitive impairment in rats in a dose dependent manner","authors":"Prasada Chowdari Gurram ,&nbsp;Suman Manandhar ,&nbsp;Sairaj Satarker ,&nbsp;Ajmal Nassar ,&nbsp;Farmiza Begum ,&nbsp;Jayesh Mudgal ,&nbsp;Devinder Arora ,&nbsp;Madhavan Nampoothiri","doi":"10.1016/j.npep.2025.102551","DOIUrl":"10.1016/j.npep.2025.102551","url":null,"abstract":"<div><div>Neuroinflammation contributes to cognitive decline in Alzheimer's disease (AD), and the neurokinin pathway has been implicated in the pathophysiology of AD. Although Substance P (SP), an endogenous ligand to the neurokinin 1 receptor (NK1R), is primarily known as a neurotransmitter, but emerging evidence indicates it has shown both pro and anti-inflammatory actions. However, the dose-dependent nature of the SP–NK1R axis’s functional role remains to be fully elucidated. In this study, we examined the effects of SP in a rat model of AD induced by lipopolysaccharide (LPS).</div><div>A dose of 150 μg/10 μl of LPS was administered through intracerebroventricular injection to induce cognitive impairment in the rats. Two doses of SP, 50 μg/kg and 500 μg/kg were administered intraperitoneally once a day for 21 days. Behavioral assessments included the Morris water maze test and novel object recognition test to investigate cognitive defects, and the open field test evaluated locomotion. Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), amyloid-beta (Aβ), acetylcholinesterase (AChE), lipid peroxidation, and catalase were estimated in the frontal cortex and hippocampus. The cAMP-responsive element-binding (CREB) protein levels in the whole brain were estimated by western blot. The LPS treatment significantly impaired cognition, increased levels of cytokines, Aβ, oxidative stress, and AChE, while decreasing CREB levels. Notably, the lower dose of SP (50 μg/kg) restored cognitive performance and markers of AD. In contrast, the higher dose of SP (500 μg/kg) failed to reverse spatial memory impairment and neuroinflammation. Thus, our data propose the dose-dependent effect of SP on neuroinflammation-induced cognitive deficits in AD.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"113 ","pages":"Article 102551"},"PeriodicalIF":2.7,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144903012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Catestatin attenuates cerebral ischemia/reperfusion injury and suppresses endoplasmic reticulum stress","authors":"Xiaodong Zhang,&nbsp;Jiaxin Fan,&nbsp;Shuyin Ma,&nbsp;Nan Zhang,&nbsp;Kaili Shi,&nbsp;Mengying Chen,&nbsp;Minyu Duan,&nbsp;Qingling Yao,&nbsp;Yuxuan Cheng,&nbsp;Shuang Du,&nbsp;Huiyang Qu,&nbsp;Han Yang,&nbsp;Tiantian Gao,&nbsp;Shuqin Zhan","doi":"10.1016/j.npep.2025.102550","DOIUrl":"10.1016/j.npep.2025.102550","url":null,"abstract":"<div><div>Ischemic stroke is one of the leading causes of death worldwide. Catestatin (CST), as a pleiotropic hormone, displays an anti-apoptotic effect, in addition to its known roles in cardiovascular regulation. However, the role of CST in ischemic stroke remains unclear. In this study, we investigated the temporal changes of CST levels in the cortex and serum of middle cerebral artery occlusion/reperfusion (MCAO/R) rats. Intracerebroventricular administration of CST significantly alleviated neurological deficits, reduced cerebral infarct volume, cerebral edema, and pathological damage, while attenuating neuronal apoptosis and modulating apoptosis-related proteins. Notably, CST suppressed endoplasmic reticulum stress (ERS) by inhibiting the PERK pathway. Furthermore, in vitro experiments using the oxygen-glucose deprivation/reperfusion (OGD/R) model of PC12 cells demonstrated that CST similarly inhibited apoptosis, as evidenced by flow cytometry and consistent changes in apoptosis-related proteins. These findings collectively demonstrate that CST exerts neuroprotective effects against cerebral ischemia-reperfusion injury (CIRI), with these effects potentially mediated through inhibition of ERS via the PERK signaling pathway.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"113 ","pages":"Article 102550"},"PeriodicalIF":2.7,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144829600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chromogranin B: A versatile neuroendocrine protein regulating physiological and metabolic functions","authors":"Chandramouli Mukherjee,&nbsp;Palki Chauksey,&nbsp;Aamna Jain,&nbsp;Bhavani S. Sahu","doi":"10.1016/j.npep.2025.102548","DOIUrl":"10.1016/j.npep.2025.102548","url":null,"abstract":"<div><div>Chromogranin B (CHGB) is a key member of the granin family of acidic proteins, predominantly localized in the secretory granules of professional secretory cells, such as neurons and neuroendocrine cells. It plays a crucial role in the regulated secretory pathway, influencing hormone storage, processing, and release. CHGB's role extends from cellular processes to systemic physiology, encompassing vesicular trafficking, calcium homeostasis, and immune regulation. CHGB dysfunction is linked to pathological conditions such as neurodegenerative diseases, cardiovascular disorders, and metabolic disorders. This review examines the multifaceted functions of CHGB at both the cellular and organismal levels, highlighting its role in maintaining cellular homeostasis and its potential link to metabolic dysfunction and related pathophysiology.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"113 ","pages":"Article 102548"},"PeriodicalIF":2.7,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144826687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}