Inflammopharmacology最新文献

{"title":"Empagliflozin and memantine combination ameliorates cognitive impairment in scopolamine + heavy metal mixture-induced Alzheimer's disease in rats: role of AMPK/mTOR, BDNF, BACE-1, neuroinflammation, and oxidative stress.","authors":"Ebtsam S Abdel-Lah, Hoda S Sherkawy, Wafaa H Mohamed, Mariam A Fawy, Asmaa A Hasan, Asmaa A Muhammed, Amira F Taha, Abeer A Tony, Nashwa Hamad, Marwa G Gamea","doi":"10.1007/s10787-025-01755-5","DOIUrl":"https://doi.org/10.1007/s10787-025-01755-5","url":null,"abstract":"<p><p>One of the major consequences of diabetes mellitus that has gained attention due to its rising incidence is cognitive impairment. Recent research suggested that sodium-glucose cotransporter-2 (SGLT-2) inhibitors can mitigate memory impairment linked to Alzheimer's disease and are now being explored for their cognitive benefits. However, their mechanisms were not thoroughly studied. This research investigates the hypothesis of the neuroprotective effect of empagliflozin administration against scopolamine-heavy metal mixture (SCO + HMM)-treated Alzheimer's rat models in comparison with memantine as a reference drug and the impact of their combination. Yet, the neuroprotective effects of memantine and empagliflozin combination against cognitive impairment have not been previously explored. This study employed adult male albino rats categorized into five groups. The impact of empagliflozin, memantine, and their concomitant administration on cognitive performance was assessed in a scopolamine and heavy metal mixture-treated Alzheimer's disease model in rats. The assessment of rats' cognitive behavior, memory, and spatial learning was conducted, followed by an evaluation of hippocampal brain-derived neurotrophic factor (BDNF), beta-secretase (BACE-1), oxidative stress (OS), and inflammatory marker activity. And, a western blot analysis was conducted to detect phosphorylated 5' AMP-activated protein kinase (p-AMPK), phosphorylated mammalian target of rapamycin (p-mTOR), and heme oxygenase-1 (HO-1). Hippocampal and cerebellar histopathology were thoroughly examined, in addition to the expressions of amyloid β (Aβ). The current data demonstrate the involvement of the pAMPK/mTOR/HO-1 signaling pathway in empagliflozin neuroprotection against SCO + HMM-induced AD. In addition, it reduces AD hallmarks (Aβ and BACE1), neuro-inflammation, and oxidative stress sequelae, and enhances neurogenesis and synaptic density via BDNF. This study proposes that EMPA, especially when co-administered with other conventional anti-Alzheimer therapy, may be formulated into an innovative therapeutic strategy for the enhancement of cognitive impairments associated with neurodegenerative disorders.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chaperone-mediated autophagy, heat shock protein 70, and serotonin: novel targets of beta-hydroxybutyrate in HFFD/LPS-induced sporadic Alzheimer's disease model.","authors":"Reem A Mohamed, Dalaal M Abdallah, Hanan S El-Abhar","doi":"10.1007/s10787-025-01754-6","DOIUrl":"https://doi.org/10.1007/s10787-025-01754-6","url":null,"abstract":"<p><p>Sporadic Alzheimer's disease (AD), which accounts for the majority of cases, is sturdily influenced by lifestyle factors such as dietary habits, obesity, and diabetes, leading to its classification as Type 3 diabetes. To model this pathological link, our AD-like model was developed by feeding Wistar male rats a high-fat diet with fructose in drinking water (HFFD) for 8 weeks, followed by a single dose of lipopolysaccharide (LPS). This group was compared with a normal control group fed a standard diet and a β-hydroxybutyrate (BHB)-treated group (125 mg/kg, p.o.), administered starting 3 h after LPS and continuing for 1 week. The results demonstrate that BHB treatment illuminated cognitive gains, as indicated by the Y-maze, Morris water maze, and novel object recognition tests. In addition, it preserved hippocampal cytoarchitecture, reduced neurodegeneration, and attenuated amyloid plaques and phosphorylated Tau deposition. Cellularly, BHB restored critical molecular mechanisms, including increased lysosomal-associated membrane protein 2A (LAMP2A) hippocampal content as the main marker of chaperone-mediated autophagy (CMA), along with the chaperon protein Hsp70. Moreover, BHB alleviated neuroinflammation by inhibiting the nucleotide-binding domain, leucine-rich-containing family, and pyrin domain-containing-3 (NLRP3) inflammasome activation alongside the downstream targets cleaved caspase-1 and IL-1β/IL-18 cytokines. BHB also reduced pyroptotic markers, caspase-11 and gasdermin-N, and microglia-induced inflammation as it shifted microglial polarization toward the neuroprotective M2 phenotype. Finally, BHB normalized hippocampal neurotransmitter levels of the inhibited acetylcholine and serotonin. These findings support BHB as a promising, multifaceted treatment for AD, highlighting the roles of CMA, Hsp70, and 5-HT in slowing disease progression and improving cognitive function.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of mGluR7 in Alzheimer's disease: pathophysiological insights and therapeutic approaches.","authors":"Garry Hunjan, Khadga Raj Aran","doi":"10.1007/s10787-025-01765-3","DOIUrl":"https://doi.org/10.1007/s10787-025-01765-3","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a progressive neurodegenerative disease characterised by oxidative stress, mitochondrial dysfunction, synaptic impairment, and neuronal loss. The progression of AD depends on two main pathologic features, amyloid-beta accumulation, and tau pathology, whereas the disruption of glutamatergic neurotransmission plays an essential role in disease progression. Glutamate, the brain's primary excitatory neurotransmitter, acts on ionotropic and metabotropic glutamate receptors (mGluRs). Metabotropic glutamate receptor 7 (mGluR7) is a pre-synaptic type III mGluR receptor playing a crucial role in the central nervous system (CNS) through neurotransmitter modulation, reducing glutamate-induced excitotoxicity, and promoting early neuronal growth. Since mGluR7 is a key regulator of neurotransmitter release, it modulates synaptic integrity and neuronal survival, and its dysfunction is associated with impaired synaptic homeostasis in AD. Moreover, mGluR7 interacts with neuroinflammatory pathways by activating microglia and regulating cytokine production, therefore playing a significant role in AD pathogenesis. The drugs targeting mGluR7, including mGluR7 agonists, antagonists, and allosteric modulators, could potentially be among the most effective agents for the treatment of psychiatric disorders, neurodegenerative diseases including AD, as well as neurodevelopmental impairments, though these potential therapies remain in the early stages. This article summarises the structure as well as the function of mGluR7 and explores current insights into the functioning of mGluR7 in molecular mechanisms of AD pathogenesis. It also discusses potential therapeutic targets of mGluR7, highlighting the need to develop such therapies to prevent disease progression.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144013128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ipomoea carnea Jacq. ameliorates formalin-induced paw inflammation in rats through modulation of oxidative and inflammatory pathways.","authors":"Shabab Nasir, Muhammad Usman, Humaira Gul, Malik Saadullah, Maryam Farrukh, Rida Siddique, Bushra Shaukat, Abdullah R Alanzi, Ana Sanches Silva, Muhammad Ajmal Shah","doi":"10.1007/s10787-025-01768-0","DOIUrl":"https://doi.org/10.1007/s10787-025-01768-0","url":null,"abstract":"<p><p>Ipomoea carnea Jacq. (I. carnea) belongs to Convolvulaceae family, that is being for the management of pain and inflammation. Since long current research was conducted to study anti-inflammatory potential of aqueous methanolic extract of Ipomoea carnea (ICE). Preliminary proximate study and HPLC were carried out for the phytochemical characterization. The safety of ICE was ensured by acute oral toxicity study. In vitro anti-inflammatory potential of ICE was evaluated using BSA denaturation methods and egg albumin. In vivo inflamed paw rat model using formalin was done at doses of 150, 300, and 600 mg/kg. Diameter of the Paw, weight changes in the body, and biochemical and hematological markers were quantified. By means of ELISA IL-6, PGE-2, TNF-α, HSP-70, SOD, CAT, and MDA levels were measured. The mRNA expression of different inflammatory genes was evaluated by qRT-PCR. Effects of ICE were noted by histological and radiological findings. Phytochemistry of ICE identified the presence of different secondary metabolic constituents and HPLC identified the various phenolic compounds in the extract. Acute oral toxicity results showed that LD₅₀ of the plant was greater than 2000 mg/kg. ICE demonstrated significant inhibition of egg albumin denaturation and protein denaturation in BSA. In vivo formalin-induced paw inflammation model demonstrated that ICE substantially decreased the severity of inflammation, in a dose-dependent manner. Hematological and biochemical parameters were improved and histological examination revealed reduction in paw inflammation, pannus formation, and bone degradation dose-dependently. The expression of pro-inflammatory genes was down-regulated with simultaneous up-regulation of anti-inflammatory genes by ICE. This study revealed that ICE possesses potent anti-inflammatory capacity thus backup its traditional use in the treatment of inflammation.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multifaceted roles of melatonin in oncology: an insight into its therapeutic potential in cancer management.","authors":"Hossein Maghsoudi, Farhad Sheikhnia, Nooshin Hajmalek, Fatemeh Dadash Gholipour, Shahriar Alipour, Mansour Ghorbanpour, Sara Farzanegan, Seyed Mostafa Mir, Mohammad Yousef Memar","doi":"10.1007/s10787-025-01751-9","DOIUrl":"10.1007/s10787-025-01751-9","url":null,"abstract":"<p><p>Cancer remains the leading cause of death worldwide. The treatment of cancer has become increasing complex. Current treatment options for cancer include surgical resection, chemotherapy, radiotherapy, nanomedicine, and immunotherapy. Recent experimental and clinical studies have provided substantial evidence supporting the potential use of melatonin as a preventive and therapeutic agent in oncology. Melatonin (N-acetyl-5-methoxy-tryptamine), a pleiotropic and multitasking molecule, is secreted from the pineal gland during the night under normal light-dark conditions. Beyond its role in circadian regulation, melatonin exhibits antioxidant, anti-aging, immunomodulatory, and anti-cancer properties. Melatonin exerts significant apoptotic, angiogenic, oncostatic, and anti-proliferative effects on a variety of cancer cells. This review discusses the influence of melatonin on cancer cells through mechanisms involving cell cycle regulation, stimulation of apoptosis, autophagy induction, epigenetic modification, and transcriptional regulation.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"2477-2492"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143977960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Flavonoids and flavonoid-based nanoparticles for the treatment of arthritis.","authors":"Sanchit Dhankhar, Jatin Kumar, Samrat Chauhan, Ishrat Zahoor, Shahid Nazir Wani, Monika Saini, Jamila Akter Borsha, Sabina Yasmin, Mohammad Yousuf Ansari","doi":"10.1007/s10787-025-01722-0","DOIUrl":"10.1007/s10787-025-01722-0","url":null,"abstract":"<p><p>Arthritis is an autoimmune disorder that predominantly causes inflammation and impacts peripheral joints. Even though immunosuppressive and NSAIDs or non-steroidal anti-inflammatory medicines are implemented for the management of this disorder, sbut they carry some severe side effects along with them. Therefore, society requires treatment with fewer side effects and powerful anti-arthritic properties, such as flavonoids. These are the most prevalent phenolic compounds found in nature that have potent antioxidant, and immunomodulatory activity and there are several bioactive flavonoids that carry potent anti-inflammatory properties. Nevertheless, only a handful has reached their clinical use. Still, in both clinical and preclinical models of arthritis, flavonoids found in the diet have been shown to reduce swelling in joints and arthritis symptoms. There are only a few scientific studies regarding their mechanisms of action in arthritis. However, the arthritic potential of dietary flavonoids is insufficient because of their limited solubility, absorption, and fast metabolism. Nanocarriers may enhance the bioavailability of flavonoids. This review examines the therapeutic effects of the most prevalent and abundant flavonoid groups on arthritis. Specifically, the modes of action of the most important flavonoids on the chemical messengers in the body that contribute to the signalling of joint inflammation-related indicators of arthritis are discussed in more detail.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"2193-2216"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of guanylate-binding protein 5 in inflammatory diseases, immune diseases, cancers, and its potential therapeutic implications.","authors":"Xufan Sun, Guiyuan Jin, Huihui Zhou, Yan Wang, Fengxian Dai, Guangxi Zhou","doi":"10.1007/s10787-025-01727-9","DOIUrl":"10.1007/s10787-025-01727-9","url":null,"abstract":"<p><p>Guanylate-binding protein 5 (GBP5) is an interferon-γ (IFN-γ)-induced GTPase (Guanosine Triphosphatease) family member. It contains highly conserved guanosine triphosphate (GTP)-binding and hydrolysis domains, particularly within myeloid and T cells. Extensive research has underscored the critical role of GBP5 in various biological processes, including inflammation, cancer cell migration, and viral defence. In addition, GBP5 is involved in a range of physiological processes and is implicated in various pathological conditions, including inflammation and immune-related disorders. Recent studies have revealed the significant role of GBP5 in the initiation and progression of cancer. The impact of GBP5 on cancer varies depending on the specific cancer type and its underlying mechanisms of action. GBP5 can modulate multiple signalling pathways, including those involved in cell proliferation, cell cycle regulation, invasive metastasis, and the maintenance of homeostasis in vivo, all of which contribute to the progression of cancer. Consequently, in addition to functioning as a downstream molecule in the IFN-γ signalling pathway, GBP5 can influence the onset and progression of various diseases. This article examines the role of GBP5 in inflammation, autoimmune disorders, and malignancies while also exploring its potential therapeutic implications. We aim to deepen our understanding of GBP5 and assess its prospective applications in clinical diagnosis and treatment.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"2217-2229"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NSAID-encapsulated nanoparticles as a targeted therapeutic platform for modulating chronic inflammation and inhibiting cancer progression: a review.","authors":"Srivarshini Sankar, Bharathi Kalidass, Janani Indrakumar, Gothandam Kodiveri Muthukaliannan","doi":"10.1007/s10787-025-01760-8","DOIUrl":"10.1007/s10787-025-01760-8","url":null,"abstract":"<p><p>Recent advancements in nanotechnology have significantly advanced nanocarrier-mediated drug delivery systems, promoting therapeutic outcomes in mitigating chronic inflammation and cancer. Nanomaterials offer significant advantages over traditional small-molecule drugs, including a high surface-area-to-volume ratio, tunable structural features, and extended bloodstream circulation time. Chronic inflammation is a well-established mechanism for malignant initiation, progression, and metastasis, promoting the potent strategy for cancer prevention and therapy. Numerous studies revealed that nonsteroidal anti-inflammatory drugs (NSAIDs) have the therapeutic ability to manage disease progression via amolerating angiogenesis and inducing apoptosis. However, prolonged intake of NSAIDs is often limited by adverse side-effects and systemic toxicities. The encapsulation of NSAIDs in a nanocarrier have materialized as a dynamic approach to mitigate the limitations by improving pharmacokinetics and pharmacodynamics, reducing off-target effects, and enhancing the drug stability. This review encompasses recent progress in the development of NSAID-based nanotherapeutics, focusing on pivotal mechanisms underlying nanoparticle-mediated drug delivery, such as improved tumor-specific targeting and strategies to overcome drug resistance. The ability of these nano-cargoes to accommodate anti-inflammatory strategies with advanced drug delivery platforms is critically evaluated. This review also highlights the transformative potential of NSAID-encapsulated nanoparticles as a multifaceted therapeutic venue for addressing chronic inflammation and mitigating cancer progression.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"2493-2522"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143999803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of corticoid receptors on Alzheimer's disease: a neuroendocrine perspective.","authors":"Falguni Goel, Daksh Kumar, Anushka Sharma","doi":"10.1007/s10787-025-01734-w","DOIUrl":"10.1007/s10787-025-01734-w","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a progressive neurodegenerative disorder that has been strongly associated with changes in corticoid receptor function and HPA axis dysregulation. This review gives an overview of the complex role of GC and MC receptors in AD, especially how chronic exposure to elevated cortisol contributes to hippocampal degeneration, oxidative stress, and cognitive decline. Specific emphasis lies with cortisol, brought to the attention of neurotoxicity, and relates it to Cushing syndrome with chronic hyper-cortisolism simulating cognitive and structural impairments seen in AD. The impact of HPA axis over-activity in AD pathology is presented, demonstrating its contribution to neuro-inflammation and possible utilization as a biomarker for disease progression. This review further includes pharmacological strategies that modulate corticoid receptors for the reduction of GC-induced neurotoxicity and includes selective GR antagonists and MR agonists. Lifestyle modifications, which modulate HPA activity, are the other non-pharmacological approach to managing AD. Finally, novel drugs and interventions targeting the regulation of GC, anti-inflammatory pathways, as well as attenuation of oxidative stress are emerging strategies. Such a strategy implies that it is possible that receptor activity balance can delay or arrest AD progression.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"2641-2656"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbial imbalance in the gut: a new frontier in Rheumatoid arthritis research.","authors":"Rufaida Wasim, Sumaiya, Asad Ahmad, Aamir Anwar, Aimen Salman","doi":"10.1007/s10787-025-01737-7","DOIUrl":"10.1007/s10787-025-01737-7","url":null,"abstract":"<p><p>A chronic autoimmune illness that causes joint destruction and inflammation, rheumatoid arthritis (RA) often results in disability. Genetic, environmental, and immune system variables all have a role in the pathophysiology of RA. The complex community of bacteria that live in the gastrointestinal system, known as the gut microbiota, has been implicated in the onset and progression of RA in recent years, according to mounting data. An imbalance in the gut microbiota's composition, known as dysbiosis, has been noted in RA patients. This imbalance may impact inflammatory pathways and immunological responses, which in turn may contribute to the development and severity of the illness. Research has shown that some bacterial species, including Firmicutes, Bacteroidetes, and Proteobacteria, are either more abundant or less prevalent in RA patients than in healthy people. The gut-immune system axis may be modulated, immunological tolerance may be affected, and pro-inflammatory cytokine production may be enhanced by these microbial changes, all of which may lead to systemic inflammation linked to RA. Moreover, changes in intestinal permeability and a rise in microbial metabolite translocation may make autoimmune reactions worse. Probiotics, antibiotics, and dietary changes have also been investigated as possible treatment approaches to help RA patients regain the balance of their gut microbiota. Still up for debate, however, are the precise ways in which the gut microbiome affects RA. Comprehending the complex connection between gut microbiota and RA may give new perspectives on managing and preventing the condition, as well as future prospects for medicines that target the microbiome.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"2277-2291"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144009302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}