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The Role of Leukemia Inhibitory Factor in Attenuating Skeletal Muscle Atrophy: Mechanisms to Exercise Interventions.
Cells
Na Jiang, Shiyi Wang, Jiaqiao Zhang +1 more
Leukemia inhibitory factor (LIF), a member of the interleukin-6 (IL-6) cytokine family, is a well-characterized myokine with pleiotropic regulatory effects on skeletal muscle. LIF modulates several fundamental cellular processes, including myoblast proliferation, apoptosis, angiogenesis, and energy metabolism. Exercise upregulates LIF expression in skeletal muscle, thereby promoting satellite cell activation, proliferation, myoblast differentiation, and angiogenesis, facilitating physiological muscle hypertrophy, and suppressing myocyte apoptosis and muscle atrophy. In addition, LIF plays a critical role in modulating the inflammatory and extracellular matrix remodeling following exercise-induced muscle damage, thereby supporting efficient muscle repair and regeneration. This review elaborates on the biological mechanisms by which LIF regulates skeletal muscle atrophy and contributes to the enhancement of skeletal muscle function. It also highlights the biological characteristics of myogenic LIF and discusses future directions for basic and applied research on exercise interventions targeting LIF signaling pathways.
Single-Cell RNA Sequencing Reveals Cellular Heterogeneity and Developmental Dynamics of Goose Satellite Cells During Embryogenesis.
Cells
Cui Wang, Yi Liu, Guitao Jiang +5 more
Skeletal muscle satellite cells (SMSCs) are essential for embryonic myogenesis and postnatal muscle regeneration; however, their cellular heterogeneity and transcriptional dynamics during avian development remain largely unexplored. Here, we performed single-cell RNA sequencing (scRNA-seq) on 42,886 cells isolated from goose leg muscles across four embryonic stages (E13, E15, E18, and E23), with each stage comprising pooled tissues from four female embryos. Unbiased clustering resolved 22 transcriptionally distinct clusters representing six major cell types-satellite cells, myocytes, fibro-adipogenic progenitors, endothelial cells, immune cells, and Schwann cells-with satellite cells being the most abundant. Satellite cells were further subdivided into three functional states (quiescent, activated, and proliferative/differentiating), which followed a continuous, linear pseudotime trajectory from early to late embryonic stages. This trajectory was marked by a progressive downregulation of stemness-associated regulators (e.g., PAX7) and upregulation of myogenic commitment and differentiation factors (e.g., MYF5, MYOD1, and MYOG), faithfully mirroring chronological development. Cell-cell communication analysis revealed that quiescent satellite cells exhibited the most extensive intercellular signaling networks (e.g., FGFR, Ephrin, collagen, CADM), whereas activated and proliferative/differentiating cells showed progressively diminished communication capacity. Across developmental stages, the contribution intensities of key signaling pathways-including SEMA6, CDH, FGF, LAMININ, MK, MPZ, CADM, FN1, and COLLAGEN-varied significantly among satellite cell states, indicating state-specific responsiveness to microenvironmental cues. Collectively, these findings demonstrate that satellite cells dynamically coordinate extrinsic signal integration with intrinsic differentiation programs to achieve orderly myogenic progression. This study provides a high-resolution single-cell atlas of goose SMSC development, uncovering subpopulation heterogeneity, state-specific molecular signatures, and key signaling pathways, with important implications for avian muscle biology and genetic improvement of poultry.
Efficacy and Safety of Oral Semaglutide in the Management of Diabetes and Obesity: A Comprehensive Meta-analysis of Real-world Evidence.
touchREV Endocrinol
Sweekruti Jena, Radhika Jindal, Deep Dutta +2 more
Oral semaglutide is the only oral glucagon-like peptide-1 receptor agonist approved for type 2 diabetes (T2D) management. Although its efficacy and safety are established from randomized controlled trials (RCTs), real-world evidence (RWE) may differ. No comprehensive systematic review and meta-analysis (SRM) has holistically analysed the RWE on oral semaglutide. This SRM analysed the RWE outcomes of oral semaglutide.
Towards Sustainable Synthesis of Peptide Therapeutics via Tag-Assisted Peptide Synthesis and Aryl Selenoester Aminolysis Ligation.
J Am Chem Soc
Peter H G Egelund, Ayman Rachid, Anthony Ayoub +7 more
There has been a recent renaissance in the use of peptides as therapeutic agents across a range of indications, sparking significant demand for the development of sustainable and cost-effective alternatives to solid-phase peptide synthesis (SPPS) for the production of these molecules, particularly in the pharmaceutical industry. While tag-assisted peptide synthesis (TAPS) has offered promise, this methodology cannot be routinely used to assemble longer peptide targets (>20 residues), limiting its utility for most peptide therapeutics. Fragment condensation of side-chain-protected peptides using coupling reagents is typically used to prepare larger targets, but this approach usually leads to unacceptable levels of epimerization without significant optimization. Herein, we report an efficient platform for the synthesis of pharmaceutically relevant peptides through direct aminolysis of peptide aryl selenoesters generated via TAPS. Notably, this novel ligation method circumvents the limitations of peptide length associated with TAPS, leads to minimal epimerization, and significantly reduces reagent and solvent use, making it attractive from an environmental standpoint. By integrating the aryl selenoester aminolysis ligation (ASAL) into the TAPS workflow, the convergent synthesis of several therapeutic peptides of increasing complexity was successfully accomplished, including osteoporosis drug teriparatide (34 residues), sulfated tsetse fly-derived thrombin-inhibiting anticoagulant TTI (32 residues), and tirzepatide (39 residues), used for the treatment of type 2 diabetes and weight management. When used in concert with TAPS, the ASAL reaction developed here can serve as a robust method for the ligation-based assembly of tagged peptides, creating a scalable route to access peptide-based therapeutics across academia and industry with a low environmental impact.
Honokiol-loaded nanomicelles reprogram senescence and immune evasion in hepatocellular carcinoma via SIRT3-mediated mitochondrial stabilization.
Bioeng Transl Med
Wenxing Deng, Yizhi Wu, Yisheng Yin +1 more
Hepatocellular carcinoma (HCC) is a major cause of cancer-related deaths. Advanced-stage patients face poor prognosis due to chemotherapy resistance and an immunosuppressive tumor microenvironment (TME). Cellular senescence, marked by the senescence-associated secretory phenotype, promotes tumor progression and immune evasion. Although honokiol (HKL) shows strong antitumor activity, its clinical use is limited by poor solubility, rapid clearance, and low bioavailability. Here, we report HKL-loaded poly(ethylene glycol)-poly(ε-caprolactone)-poly(ethylene glycol) triblock copolymer nanomicelles (HKL-nm) as a multifunctional nanotherapeutic platform. HKL-nm exhibited a uniform spherical shape with a diameter of 60.93 ± 5.7 nm, near-neutral charge (-0.28 ± 0.1 mV), and high encapsulation efficiency (85.9 ± 4.9%). It enabled sustained drug release (70.04 ± 6.2% over 200 h) and significantly improved oral pharmacokinetics (area under the curve increased 6.26-fold and C max increased 4.06-fold). Specifically, the HKL drug concentration at the tumor site was enhanced by 3.52-fold. Mechanistically, HKL-nm suppressed senescence markers (p53, p16, and p21) and senescence-associated β-galactosidase positivity via a Sirtuin 3-dependent pathway, inhibiting cytoplasmic mitochondrial DNA leakage and cGAS-STING signaling. In Hepa1-6 cells xenografts, combination therapy with HKL-nm and the senolytic cocktail dasatinib + quercetin achieved tumor volume reduction, with transcriptomic analysis validating enrichment of immune activation pathways. This was accompanied by enhanced infiltration of CD8+ cytotoxic T cells and mature dendritic cells, coupled with profound suppression of myeloid-derived suppressor cells. By integrating nanodelivery, senescence modulation, and immuno-oncology, HKL-nm represents a promising strategy to overcome therapeutic resistance in HCC, providing a preclinical basis for translation to solid tumors.
Long-Distance Trail Running Induces Inflammatory-Associated Protein, Lipid, and Purine Oxidation in Red Blood Cells.
Blood Red Cells Iron
Travis Nemkov, Emeric Stauffer, Francesca Cendali +10 more
Ultra-endurance running imposes extreme demands on oxygen transport, yet how red blood cells (RBCs) respond at the molecular level remains poorly defined. We integrated plasma and RBC multi-omics with hematology and hemorheology in athletes sampled before and after two trail races of distinct duration: a 40-km marathon (MCC) and a 171-km ultramarathon (UTMB). Both races elicited systemic inflammation, but UTMB was distinguished by marked IL-6 and kynurenine increases, acute-phase protein induction, and profound lipid remodeling. In RBCs, acylcarnitine accumulation, pantothenate depletion, and oxidized lipid species indicated Lands cycle activation, while purine salvage and carboxylate metabolism reflected redox-sensitive rerouting of energy pathways. Proteomics revealed non-random oxidation, particularly methionine oxidation of antioxidant enzymes, metabolic proteins, and proteasome components, correlating with impaired deformability as gleaned by testing of rheological properties. Elevated copper provided an additional correlate of reduced RBC mechanics. Despite minimal signatures of intravascular hemolysis, plasma bilirubin and hypoxanthine rose, consistent with extravascular clearance of damaged RBCs. Collectively, these results demonstrate that ultra-running accelerates RBC aging through inflammatory and oxidative pathways beyond mechanical trauma, linking systemic cytokine responses to molecular lesions, biomechanical dysfunction, and splenic sequestration. These findings not only identify actionable biomarkers of exercise-induced hemolysis but also provide translational insight into oxidative lesions that similarly limit RBC survival in transfusion and inflammatory disease settings.
Bridging aging and colorectal cancer: synergistic roles of inflammaging and immunosenescence.
Front Immunol
Silvere D Zaongo, Qiyu Yang, Mei Han +5 more
Colorectal cancer (CRC) is one of the most commonly occurring malignancies worldwide, with incidence and mortality rising sharply in older adults. While aging is increasingly recognized as a key risk factor for CRC, the fundamental immunological mechanisms which underlie this risk remain incompletely understood. Two interconnected processes, namely inflammaging and immunosenescence, appear central to this association. On the one hand, inflammaging, which is characterized by chronic low-grade inflammation in older individuals, fosters a tumor-promoting microenvironment through oxidative stress, genomic instability, and persistent cytokine activation. On the other hand, immunosenescence diminishes immune surveillance, reducing the clearance of premalignant cells and weakening responses to tumor progression and therapy. Together, these processes create an immunological framework that predisposes the aging colon to malignant transformation. This review synthesizes current knowledge of the cellular and mechanistic impacts of inflammaging and immunosenescence in CRC pathogenesis, highlighting their roles in shaping disease susceptibility in the elderly. These insights may guide future endeavor in biomarker discovery, prevention, and therapeutic intervention to mitigate the burden of CRC in aging populations.
Mechanisms by Which Exercise Delays Brain Aging Through Regulation of the Mitochondrial Quality Control System.
Biology (Basel)
Xinyi Zhu, Lei Shi, Yahong Dong +2 more
Brain aging is a complex biological process characterised by progressive neuronal and synaptic decline, in which disruption of mitochondrial quality control plays a central role. This system encompasses multiple synergistic components, including mitochondrial biogenesis, dynamic equilibrium, autophagic clearance, and energy metabolism. Aging induces dysfunction across these processes, precipitating mitochondrial fragmentation, functional decline, and energy crises, ultimately driving cognitive deterioration. Exercise is a promising non-pharmacological intervention for preserving brain health during aging, and its benefits may be mediated, at least in part, through modulation of mitochondrial quality control. Specifically, exercise has been shown to activate key signaling pathways such as AMPK/SIRT1/PGC-1α, thereby promoting mitochondrial biogenesis and metabolic adaptation. It may also regulate mitochondrial dynamics and mitophagy via pathways including cAMP/PKA/Drp1 and AMPK/mTOR. In addition, emerging evidence indicates that exercise may influence brain mitochondrial function through activity-dependent regulation of mitochondrial gene expression and systemic signaling factors. Furthermore, this review discusses potential differences between exercise modalities and highlights future directions for personalised intervention strategies, providing a theoretical basis for the application of exercise in delaying brain aging and preventing neurodegenerative diseases.
Network pharmacology and experimental evaluation of Sanwei Tanxiang Tangsan in doxorubicin-induced heart failure.
J Cardiothorac Surg
Davaadagva Aruna, Battulga Dulan, Hua Damdinjav +3 more
Heart failure (HF) is a complex syndrome characterized by inflammation, oxidative stress, and cardiomyocyte apoptosis, for which effective and well-tolerated therapies remain limited. This study sought to explore the potential mechanisms by which Mongolian medicine Sanwei Tanxiang Tangsan (STX) may be associated with AKT1/p53-related signaling in the mitigation of HF, employing network pharmacology, molecular docking, and animal experimentation.
Extreme Heterophilic Antibody Interference in BNP Immunoassay: A Case Report and Systematic Investigation Protocol.
J Clin Lab Anal
Huicong Yang, Yuanhai Zheng, Zhenhua Zeng +4 more
Heterophilic antibody (HA) interference remains a persistent challenge in immunoassay diagnostics. Human anti-mouse antibodies (HAMA) can cause spuriously elevated biomarker results, potentially leading to misdiagnosis and unnecessary clinical interventions. Brain natriuretic peptide (BNP) is critical for heart failure diagnosis, but false-positive results due to HAMA may trigger inappropriate clinical management.
Neuroendocrine Regulation of Female Fertility: The Role of CNS-Derived Hormones.
J Mol Endocrinol
Amirreza Shakoeizadeh, Erfan Shahabinejad, Mahdi Heydari +2 more
Infertility is an increasing concern for many women and can affect both physical and emotional well-being. The central nervous system (CNS) -particularly the hypothalamus, pituitary gland, and pineal gland - plays a crucial role in female reproductive health. We conducted a narrative review of relevant studies published between 2015 and 2025, sourcing data from PubMed and Scopus. Our goal was to investigate how dysregulation of hormones from the hypothalamus, pituitary gland, and pineal gland contributes to fertility-related disorders, such as impairments in ovulation, oocyte quality, and embryo development. Both human and significant animal studies were considered to better understand how CNS hormones affect fertility. The findings emphasize the roles of key hormones, including gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), melatonin, Adrenocorticotropic Hormone (ACTH), Thyroid-Stimulating Hormone (TSH), and vasopressin (ADH). The proper timing and balance of these hormones are vital. For instance, GnRH pulses regulate the release of LH and FSH, which are essential for ovulation and follicle development. Melatonin supports oocyte health and helps maintain the menstrual cycle, while ACTH and TSH are also involved in reproductive function. Vasopressin contributes by affecting uterine activity and hormone production. Understanding these hormonal interactions may lead to better diagnostic tools and more effective treatment strategies for conditions such as polycystic ovary syndrome (PCOS) and other fertility-related disorders. Unlike previous studies, this research provides a comprehensive investigation of how CNS-mediated hormonal regulation influences female reproductive outcomes, examining the roles of all involved hormones.
Alternating Therapy With Osilodrostat and Etomidate in Severe Ectopic Cushing's Syndrome Complicated by Silent Bowel Perforation.
Case Rep Endocrinol
Hery Mejia, Carmen Villabona, Renato Savian +7 more
Ectopic adrenocorticotropic hormone (ACTH)-dependent Cushing's syndrome (CS), ectopic ACTH secretion (EAS) is a rare condition caused by ACTH-secreting neuroendocrine tumors (NETs), such as bronchial carcinoids. We report a 65-year-old woman with severe EAS complicated by bowel perforation. She presented with hypokalemia (K+ 2.3 mmol/L), metabolic alkalosis, resistant hypertension (180/110 mmHg), worsening diabetes (HbA1c 6.7%-9.1%), proximal muscle weakness, and 14 kg weight gain over 3 months. A silent sigmoid colon perforation required emergency resection and colostomy. Biochemical tests confirmed hypercortisolism (urine free cortisol [UFC], 1256 µg/24 h, plasma ACTH 175 pg/mL, and cortisol >40 µg/dL post-dexamethasone). Imaging identified a 2.3 cm pulmonary nodule with mild uptake on Ga-68 DOTATATE PET/CT. Bronchoscopic biopsy confirmed an ACTH-positive low-grade bronchial carcinoid tumor. Initial treatment with osilodrostat was interrupted due to acute illness and oral medication intolerance. Intravenous etomidate was employed in the ICU for rapid cortisol suppression, followed by resumption of osilodrostat after stabilization. Thoracoscopic lobectomy confirmed a low-grade carcinoid tumor (Ki-67 < 2%). Postoperatively, cortisol normalized, electrolytes stabilized, and HbA1c improved to 6.5%. This case highlights bowel perforation as a severe complication of EAS and underscores the importance of dynamic, alternating therapy with osilodrostat and etomidate, along with individualized surgical and medical management strategies.
The Role of High-Protein Instant Ramen Noodles in Inducing and Maintaining Satiety: Acute, Randomized, Crossover Study.
Nutr Diabetes
Princess U Ozioma, Gaurav M Kudchadkar, Sara Ranjbar +6 more
This study tested if a breakfast meal of high-protein instant ramen noodles would increase satiety, reduce hunger, improve glycemic response, and reduce lunch-time energy intake compared to an isocaloric breakfast of standard protein instant ramen noodles.
Magnetic enrichment and enabled cascade amplification for ultrasensitive SPR analysis of PD-L1+ exosomes.
Biosens Bioelectron
Hezhen Liu, Zhaofei Liu, Kwangnak Koh +1 more
Exosomes serve as stable liquid-biopsy biomarkers for early cancer detection due to their molecular resemblance to parent cells. Here, a magnetic enrichment-assisted surface plasmon resonance (SPR) assay is developed based on Zr/Ce-MOF@Fe3O4 core-satellite nanocomposites for sensitive exosome analysis. The Zr/Ce-MOF is constructed with Zr as the metal node and doped with Ce, exhibiting intrinsic oxidase-like activity through the Ce3+/Ce4+ redox cycle. It catalyzes the oxidation of 3,3',5,5'-tetramethylbenzidine without exogenous H2O2, generating a high-refractive-index precipitate that significantly amplifies the SPR signal. The Zr-O-P coordination enables selective capture of phospholipid membranes on exosomes, while Fe3O4 satellites facilitate rapid magnetic enrichment and separation. To further improve specificity and antifouling performance, single-walled carbon nanotube interlayers pre-functionalized with PD-L1 targeting peptides were integrated onto the sensor chip, enabling selective recognition of magnetically enriched PD-L1+ exosomes. The combined refractive-index increase from the nanocomposite and the TMB deposition leads to enhanced SPR responses. Under optimized conditions, the assay achieves a detection limit of 2.16 particles mL-1 (S/N = 3) over a linear range of 102-107 particles mL-1. The total analysis time is within 40 min, and the method shows consistent differentiation between serum samples from cancer patients and healthy donors. This approach provides a practical strategy for the analysis of low abundance exosomal biomarkers.
Cost-effectiveness of semaglutide versus dulaglutide for Type 2 Diabetes in China: A Markov Model analysis.
PLoS One
Qiying Chen, Tianyu Chen, Weicheng Lin +1 more
From the perspective of China's basic medical insurance, to evaluate the cost-effectiveness of semaglutide versus dulaglutide for type 2 diabetes mellitus (T2DM) in China, informing clinical and health policy decisions.
GLP-1 receptor agonist adjunct therapy stabilises Ramadan dysglycaemia in insulin-treated diabetes: a CGM-based study.
Diabetes Res Clin Pract
Tanveer Ashraf, Nader Lessan
Patients with type 1 and insulin-treated type 2 diabetes are at higher risk of hypo- and hyperglycaemia during Ramadan fasting. The role of incretin-based add-on therapy (GLP-1 receptor agonist semaglutide and the GLP-1/GIP dual agonist tirzepatide) in attenuating Ramadan dysglycaemia in insulin-treated type 2 diabetes has not been characterised using continuous glucose monitoring. Emerging evidence indicates that exaggerated post-iftar hyperglycaemia, drives Ramadan dysglycaemia in insulin-treated individuals.
Microbiota-driven gut-brain signaling underlies antidepressant effects of a GLP-1 analog.
Cell Host Microbe
Liang Bian, Yang Cai, Yuan Zhang +11 more
Despite widespread clinical use of glucagon-like peptide-1 receptor (GLP-1R) agonists for metabolic disease, their neuropsychiatric effects remain poorly understood and controversial. Here, we demonstrate that liraglutide alleviates depression through a gut-brain pathway that operates independently of GLP-1R. Using both pharmacological and genetic approaches, we demonstrated that liraglutide retained antidepressant efficacy in GLP-1R antagonist-Exn9-treated mice or in Glp1r-/- mice, whereas gut microbiota depletion abolished its effects. Multi-omics analyses revealed that liraglutide increased the abundance of Lactobacillus delbrueckii, which in turn restored the levels of the endocannabinoid 2-arachidonoylglycerol (2-AG). The elevation of 2-AG mediated the antidepressant effects by normalizing excessive neuronal activity in emotional processing brain regions. Importantly, fecal microbiota transplantation from liraglutide-treated mice or Lactobacillus delbrueckii colonization replicated the antidepressant effects. These findings uncover a non-canonical mechanism of action for GLP-1 analogs, highlighting a specific microbiota-endocannabinoid metabolic pathway as a potential therapeutic target for depression.
Cerebral hypoperfusion and the vascular-metabolic-immune-glymphatic network in Alzheimer's disease: mechanisms, diagnosis, and therapy.
Neuroscience
Mingyuan Yao, Annan Liu, Jing Song +3 more
Alzheimer's disease (AD), characterized by progressive cognitive decline, represents a major public health challenge in aging societies. Since the proposal of the amyloid cascade hypothesis, Aβ-targeted therapeutic strategies have dominated this field for over three decades. Although recent anti-Aβ antibodies have shown modest promise, their limited clinical benefits coupled with safety concerns underscore the necessity of re-evaluating the pathological mechanisms underlying AD. Cerebral hypoperfusion (CH), a detectable alteration emerging in the preclinical stage of AD, has garnered increasing attention for its potential driving role in disease pathogenesis. This review proposes a "vascular-metabolic-immune-glymphatic" (VMIG) pathological network model originating from CH: CH induces pericyte damage, astrocyte end-feet impairment, and extracellular matrix degradation, thereby resulting in neurovascular unit dysfunction; reduces oxygen and glucose delivery, precipitating mitochondrial energy failure and reactive oxygen species overproduction, which in turn initiates neuroinflammatory cascades; and attenuates arterial pulsation-driven flow while disrupting perivascular space architecture, culminating in glymphatic system clearance dysfunction. These mechanisms are intricately interconnected, establishing a self-perpetuating pathological loop. Building upon the VMIG framework, this review integrates multimodal neuroimaging techniques (ASL-MRI, Aβ/tau-PET, DTI-ALPS) with peripheral biomarkers (VEGF/Ang-2, sTREM2/GFAP, sPDGFRβ/Aβ42 ratio) to establish a comprehensive system for early diagnosis and stratified assessment of AD. Furthermore, we advocate for temporally sequenced combinatorial therapeutic strategies targeting the pathological network and discuss the translational potential of nanoparticle-based co-delivery systems. The VMIG model offers an integrative framework for understanding the multi-system dysregulation inherent to AD, facilitating a paradigm shift from single-target intervention toward network-based restoration.
Apelin-13 activates the BMP4/SMAD pathway through APJ to enhance osteoblastic differentiation and mineralization.
Tissue Cell
Chunyan Wang, Zhanyu Li, Hongmei Yang +3 more
Osteoblastic differentiation and mineralization are essential processes for bone formation and remodeling. Apelin, an endogenous ligand for the Apelin receptor (APJ), has been involved in various physiological functions, however, its function in osteogenesis remains unclear. The present research was dedicated to exploring the impacts of Apelin-13 on the osteoblastic differentiation process within MC3T3-E1 cells. The results showed that APJ expression was upregulated during osteogenic induction. Apelin-13 greatly increased the expression of osteogenic markers ALP, OCN, OPN, and Col1A1, promoted ALP activity and mineralization, and raised RUNX-2 expression at both mRNA and protein levels. Furthermore, Apelin-13 activated the BMP4/SMAD1/5/8 signaling pathway. These effects were abolished by LDN193189, a specific inhibitor of BMP signaling, and by APJ knockdown, indicating that Apelin-13 exerts its pro-osteogenic effects through APJ via the BMP4/SMAD pathway.
Efficacy of Sacubitril/Valsartan in Treating Hemodialysis Patients with Reduced Ejection Fraction Heart Failure: A Retrospective Study.
Iran J Kidney Dis
Yan Guo, Weihua Li, Zongli Diao
Heart failure with reduced ejection fraction (HFrEF) is a prevalent and challenging complication among patients undergoing hemodialysis. Sacubitril/Valsartan (Sac-Val), an angiotensin receptor-neprilysin inhibitor, has shown promise in improving cardiac outcomes in HFrEF patients. This study aims to evaluate the efficacy and safety of Sac-Val in treating HFrEF in patients undergoing hemodialysis.