Interaction between lncRNAs and RNA-binding proteins (RBPs) influences DNA damage response in cancer chemoresistance.

The DNA damage response (DDR) is a crucial cellular signaling pathway activated in response to DNA damage, including damage caused by chemotherapy. Chemoresistance, which refers to the resistance of cancer cells to the effects of chemotherapy, poses a significant challenge in cancer treatment. Understanding the relationship between DDR and chemoresistance is vital for devising strategies to overcome this resistance and improve treatment outcomes. Long non-coding RNAs (lncRNAs) are a class of RNA molecules that do not code for proteins but play important roles in various biological processes, including cancer development and chemoresistance. RNA-binding proteins (RBPs) are a group of proteins that bind to RNA molecules and regulate their functions. The interaction between lncRNAs and RBPs has been found to regulate gene expression at the post-transcriptional level, thereby influencing various cellular processes, including DDR signaling pathways. Multiple studies have demonstrated that lncRNAs can interact with RBPs to modulate the expression of genes involved in cancer chemoresistance by impacting DDR signaling pathways. Conversely, RBPs can regulate the expression and function of lncRNAs involved in DDR. Exploring these interactions can provide valuable insights for the development of innovative therapeutic approaches to overcome chemoresistance in cancer patients. This review article aims to summarize recent research on the interaction between lncRNAs and RBPs during cancer chemotherapy, with a specific focus on DDR pathways.

Co-treatment with bone marrow-derived mesenchymal stem cells and curcumin improved angiogenesis in myocardium in a rat model of MI.

BACKGROUND: The cardioprotective properties of mesenchymal stem cells and the therapeutic potential of curcumin (CUR) have been explored. Combining these approaches may enhance stem cell effectiveness and expedite healing. This study aimed to investigate the synergistic effects of co-treating bone marrow mesenchymal stem cells (BMSCs) with curcumin on vascular endothelial growth factor (VEGF) levels, in a rat model of myocardial ischemia (MI). METHODS AND RESULTS: Sixty-five male rats were divided into four groups: G1 (healthy control), G2 (MI induced by isoproterenol hydrochloride), G3 (treated with BMSCs), and G4 (co-treated with curcumin and BMSCs). Blood and tissue samples were collected at specific time points (day 1, 7, 15 and 21) after MI induction. Serum levels of lactate dehydrogenase (LDH), creatine kinase (CK), cardiac troponin I (cTnI), aspartate aminotransferase (AST), CK-MB and VEGF were measured. VEGF mRNA and protein expression were evaluated using RT-qPCR and Western blot techniques. Histopathological assessments were performed using H&E staining and CD31 immunofluorescence staining. VEGF expression significantly increased on days 7 and 15 in the CUR-BMSCs group, peaking on day 7. Western blot analysis confirmed elevated VEGF protein expression on days 7 and 15 post-MI. ELISA results demonstrated increased serum VEGF levels on days 7 and 15, reaching the highest level on day 7 in CUR-BMSCs-treated animals. Treated groups showed lower levels of LDH, AST, CK, CK-MB and cTnI compared to the untreated MI group. H&E staining revealed improved myocardial structure, increased formation of new capillaries, in both treatment groups compared to the MI group. CONCLUSION: Combining curcumin with BMSCs promotes angiogenesis in the infarcted myocardium after 15 days of MI induction. These findings suggest the potential of this combined therapy approach for enhancing cardiac healing and recovery.

Antioxidant therapy against TGF-ß/SMAD pathway involved in organ fibrosis.

Fibrosis refers to excessive build-up of scar tissue and extracellular matrix components in different organs. In recent years, it has been revealed that different cytokines and chemokines, especially Transforming growth factor beta (TGF-ß) is involved in the pathogenesis of fibrosis. It has been shown that TGF-ß is upregulated in fibrotic tissues, and contributes to fibrosis by mediating pathways that are related to matrix preservation and fibroblasts differentiation. There is no doubt that antioxidants protect against different inflammatory conditions by reversing the effects of nitrogen, oxygen and sulfur-based reactive elements. Oxidative stress has a direct impact on chronic inflammation, and as results, prolonged inflammation ultimately results in fibrosis. Different types of antioxidants, in the forms of vitamins, natural compounds or synthetic ones, have been proven to be beneficial in the protection against fibrotic conditions both in vitro and in vivo. In this study, we reviewed the role of different compounds with antioxidant activity in induction or inhibition of TGF-ß/SMAD signalling pathway, with regard to different fibrotic conditions such as gastro-intestinal fibrosis, cardiac fibrosis, pulmonary fibrosis, skin fibrosis, renal fibrosis and also some rare cases of fibrosis, both in animal models and cell lines.

The amelioration of ovarian dysfunction by hesperidin in malathion-treated mice through the overexpression of PCNA and FSHR proteins.

Objective: Malathion (MAL), a pesticide used for decades, is a highly toxic substance. Several studies have documented the negative effects of such agents on reproductive organ physiology, but the precise mechanism of action in the induction of ovarian dysfunction remains unclear. Therefore, the purpose of this research was to examine the effects of the antioxidant hesperidin (HES) on ovarian damage and toxicity caused by malathion. Materials and methods: In this experiment, forty adult female bulb/c mice weighing 27-30 g were categorized into four groups, namely hesperidin (20 mg/kg, i.p.), malathion (3 mg/kg, i.p.), malathion + hesperidin, and control groups. Following a period of 35 consecutive days of treatment, mice were euthanized, and their ovarian tissues were gathered for the purposes of histopathological analysis by H&E staining, immunohistochemical assessment via proliferating cell nuclear antigen (PCNA) and follicle-stimulating hormone receptor (FSHR) immunostaining, and biochemical evaluation via measuring the levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1ß). In addition, serum samples were collected from the blood of mice to perform hormonal analyses, especially 17ß-estradiol (E2), progesterone (P4), luteinizing hormone (LH), and follicle-stimulating hormone (FSH). Results: The results demonstrated that MAL exposure resulted in the development of abnormalities in the architecture and structure of ovaries. Also, the treatment of mice with MAL led to declined follicular counts at all three stages, namely, primary, secondary, and tertiary, reduced serum levels of sex hormones, decreased immunoreactivity of FSHR and PCNA, and diminished activity of CAT and SOD enzymes. In contrast, it caused an increase in MDA, IL-1ß, and TNF-α, as well as the count of atretic follicles. Nonetheless, it was observed that HES exhibited the ability to ameliorate the deleterious impacts of malathion across all the aforementioned parameters. Conclusion: Treatment with HES via upregulating the protein expression of PCNA and FSHR and activating antioxidant defense was able to ameliorate the adverse effects of MAL on ovarian tissues.

LncRNA SNHG12: A budding star in human diseases.

Small nucleolar RNA host gene 12 (SNHG12) is a long non-coding RNA (lncRNA) that contributes in a variety of human pathologies. This lncRNAs acts as molecular sponge for various miRNAs, namely miR-200c-5p, miR-129-5p, miR-30a-3p, miR-195, miR-133b, miR-199a/b-5p, miR-320b, miR-16, miR-15a, miR-218-5p, miR-320 and a number of other miRNAs. Through this mechanism, SNHG12 can affect activity of HIF-1α, Wnt/ß-catenin, VEGF, PI3K/AKT/mTOR, PTEN, NF-κB and ERK-1/2 signaling. SNHG12 can affect pathogenesis of several disorders, including those arising from genitourinary, gastrointestinal, pulmonary, central nervous and cardiovascular systems. These effects have been best characterized in the context of cancer where it can be used as a possible diagnostic and prognostic marker. In order to summarize the role of this lncRNA in human disorders, particularly cancer and highlight its potential application in biomedical studies, we designed the current review. We also emphasized on its diagnostic and prognostic roles.

Non-coding RNA profile for natural killer cell activity.

Natural killer cells (NK cells) are a type of cytotoxic lymphocytes which are involved in innate immunity, alongside with assisting with adaptive immune response. Since they have cytotoxic effects, disruptions in their functionality and development leads to a variety of conditions, whether malignant or non-malignant. The profile and interaction of these non-coding RNAs and NK cells in different conditions is extensively studied, and it is now approved that if dysregulated, non-coding RNAs have detrimental effects on NK cell activity and can contribute to the pathogenesis of diverse disorders. In this review, we aim at a thorough inspection on the role of different non-coding RNAs on the activity and development of NK cells, in a broad spectrum of conditions, including blood-related disorders, viral infections, neurological diseases, gastrointestinal disorders, lung disorders, reproductive system conditions and other types of maladies, alongside with providing insight to the future non-coding RNA-NK cell studies.

The effects of whey protein on blood pressure: A systematic review and dose-response meta-analysis of randomized controlled trials.

AIMS: This systematic review and dose-response meta-analysis was conducted to summarize data from available clinical trials on the effects of whey protein (WP) supplementation on blood pressure (BP) in adults. DATA SYNTHESIS: A comprehensive literature search was conducted in the electronic databases PubMed, Web of Science, ProQuest, Embase, and SCOPUS from inception to October 2022. Weighted mean differences (WMD) and 95% confidence intervals (CI) were calculated to assess pooled effect sizes. Heterogeneity between studies was assessed using the Cochran's Q test and I2. Subgroup analysis was performed to assess potential sources of heterogeneity. The dose-response relationship was assessed using fractional polynomial modeling. Of the 2,840 records, 18 studies with 1,177 subjects were included. Pooled analysis showed that whey protein supplementation resulted in a significant reduction in systolic blood pressure (WMD: -1.54 mmHg; 95% CI: -2.85 to -0.23, p = 0.021), with significant heterogeneity between studies (I2 = 64.2%, p < 0.001), but not for diastolic blood pressure (DBP) (WMD: -0.27 mmHg; 95% CI: -1.14, 0.59, p = 0.534) with high heterogeneity between studies (I2 = 64.8%, p < 0.001). However, WP supplementation significantly reduced DBP at a dose of ˃30 g/day, in RCTs that used WP isolate powder for their intervention, in sample sizes ≤100, in studies with an intervention duration of ≤10 weeks, and in those studies that were conducted in patients with hypertension and had participants with a BMI of 25-30 kg/m2. CONCLUSION: This meta-analysis demonstrated that WP intake significantly reduced SBP levels. Further large-scale studies are needed to specify the exact mechanism, and optimal dosage of WP supplementation to obtain a beneficial effect on BP.

Nanoparticle-mediated delivery of microRNAs-based therapies for treatment of disorders.

miRNAs represent appropriate candidates for treatment of several disorders. However, safe and efficient delivery of these small-sized transcripts has been challenging. Nanoparticle-based delivery of miRNAs has been used for treatment of a variety of disorders, particularly cancers as well as ischemic stroke and pulmonary fibrosis. The wide range application of this type of therapy is based on the important roles of miRNAs in the regulation of cell behavior in physiological and pathological conditions. Besides, the ability of miRNAs to inhibit or increase expression of several genes gives them the superiority over mRNA or siRNA-based therapies. Preparation of nanoparticles for miRNA delivery is mainly achieved through using protocols originally developed for drugs or other types of biomolecules. In brief, nanoparticle-based delivery of miRNAs is regarded as a solution for overcoming all challenges in the therapeutic application of miRNAs. Herein, we provide an overview of studies which used nanoparticles as delivery systems for facilitation of miRNAs entry into target cells for the therapeutic purposes. However, our knowledge about miRNA-loaded nanoparticles is limited, and it is expected that numerous therapeutic possibilities will be revealed for miRNA-loaded nanoparticles in future.

The interaction between miRNAs and hazardous materials.

Toxic agents are broadly present in the environment, households, and workplaces. Contamination of food and drinking water with these agents results in entry of these materials to the body. The crosstalk between these agents and microRNAs (miRNAs) affects pathoetiology of several disorders. These agents can influence the redox status, release of inflammatory cytokines and mitochondrial function. Altered expression of miRNA is involved in the dysregulation of several pathophysiological conditions and signaling pathways. These molecules are also implicated in the adaption to environmental stimuli. Thus, the interactions between miRNAs and toxic materials might participate in the hazardous effects of these materials in the body. This review describes the effects of the toxic materials on miRNAs and the consequences of these interactions on the human health.

Interaction between SIRT1 and non-coding RNAs in different disorders.

SIRT1 is a member of the sirtuin family functioning in the process of removal of acetyl groups from different proteins. This protein has several biological functions and is involved in the pathogenesis of metabolic diseases, malignancy, aging, neurodegenerative disorders and inflammation. Several long non-coding RNAs (lncRNAs), microRNAs (miRNAs) and circular RNAs (circRNAs) have been found to interact with SIRT1. These interactions have been assessed in the contexts of sepsis, cardiomyopathy, heart failure, non-alcoholic fatty liver disease, chronic hepatitis, cardiac fibrosis, myocardial ischemia/reperfusion injury, diabetes, ischemic stroke, immune-related disorders and cancers. Notably, SIRT1-interacting non-coding RNAs have been found to interact with each other. Several circRNA/miRNA and lncRNA/miRNA pairs that interact with SIRT1 have been identified. These axes are potential targets for design of novel therapies for different disorders. In the current review, we summarize the interactions between three classes of non-coding RNAs and SIRT1.

Different types of bisphenols alter ovarian steroidogenesis: Special attention to BPA.

Endocrine disruptors such as bisphenol A (BPA) and some of its analogues, including BPS, BPAF, and BPE, are used extensively in the manufacture of plastics. These synthetic chemicals could seriously alter the functionality of the female reproductive system. Although the number of studies conducted on other types of bisphenols is smaller than the number of studies on BPA, the purpose of this review study was to evaluate the effects of bisphenol compounds, particularly BPA, on hormone production and on genes involved in ovarian steroidogenesis in both in vitro (human and animal cell lines) and in vivo (animal models) studies. The current data show that exposure to bisphenol compounds has adverse effects on ovarian steroidogenesis. For example, BPA, BPS, and BPAF can alter the normal function of the hypothalamic-pituitary-gonadal (HPG) axis by targeting kisspeptin neurons involved in steroid feedback signals to gonadotropin-releasing hormone (GnRH) cells, resulting in abnormal production of LH and FSH. Exposure to BPA, BPS, BPF, and BPB had adverse effects on the release of some hormones, namely 17-ß-estradiol (E2), progesterone (P4), and testosterone (T). BPA, BPE, BPS, BPF, and BPAF are also capable of negatively altering the transcription of a number of genes involved in ovarian steroidogenesis, such as the steroidogenic acute regulatory protein (StAR, involved in the transfer of cholesterol from the outer to the inner mitochondrial membrane, where the steroidogenesis process begins), cytochrome P450 family 17 subfamily A member 1 (Cyp17a1, which is involved in the biosynthesis of androgens such as testosterone), 3 beta-hydroxysteroid dehydrogenase enzyme (3ß-HSD, involved in the biosynthesis of P4), and cytochrome P450 family 19 subfamily A member 1 (Cyp19a1, involved in the biosynthesis of E2). Exposure to BPA, BPB, BPF, and BPS at prenatal or prepubertal stages could decrease the number of antral follicles by activating apoptosis and autophagy pathways, resulting in decreased production of E2 and P4 by granulosa cells (GCs) and theca cells (TCs), respectively. BPA and BPS impair ovarian steroidogenesis by reducing the function of some important cell receptors such as estrogens (ERs, including ERα and ERß), progesterone (PgR), the orphan estrogen receptor gamma (ERRγ), the androgen receptor (AR), the G protein-coupled estrogen receptor (GPER), the FSHR (follicle-stimulating hormone receptor), and the LHCGR (luteinizing hormone/choriogonadotropin receptor). In animal models, the effects of bisphenol compounds depend on the type of animals, their age, and the duration and dose of bisphenols, while in cell line studies the duration and doses of bisphenols are the matter.

Comparison of mouse ovarian follicular development and gene expression in the presence of ovarian tissue extract and sodium selenite: An experimental study.

Background: Ovarian tissue extract (OTE) and sodium selenite (SS) enhance the growth and maturation of preantral follicles in a dose-dependent manner. Objective: The present study was designed to bring more information regarding the mechanism of OTE and SS on the mRNA expression of follicle-stimulating hormone receptors (FSHR) and the proliferation cell nuclear antigens (PCNA) of in vitro matured isolated follicles. Materials and Methods: The tissue extract was prepared from adult ovaries. The preantral follicles (n = 266) were isolated from 12-16-day-old mice and cultured in the control, experimental I (10 ng/ml SS), and experimental II (OTE) groups for 12 days. The follicular diameter, survival, and maturation rates, also, the production of 17-ß-estradiol and progesterone, and the follicular expression of PCNA and FSH receptor genes were analyzed. Results: The survival rate of follicles in the SS-treated group (84.58%) was significantly higher than that OTE (75.63%; p = 0.023) and control (69.38%; p = 0.032) groups. The mean diameter of culture follicles in experimental group I (403.8 µm) and experimental group II (383.97 µm) increased significantly in comparison with the control group (342.05 µm; p = 0.032). The developmental rate of follicles, percentages of antrum formation, released metaphase II oocytes (p = 0.027; p = 0.019 respectively), production of hormones and the expression of 2 studied genes were significantly increased in both experimental groups in compare with control group (p = 0.021; p = 0.023 respectively). Conclusion: The OTE and SS have a positive effect on development of mouse preantral follicles via over-expression of FSHR and PCNA genes.

Corrigendum to "Protective effects of chlorogenic acid against ionizing radiation-induced testicular toxicity" [Heliyon 8 (10) (October 2022) Article e10798].

[This corrects the article DOI: 10.1016/j.heliyon.2022.e10798.].

Emerging functions and clinical applications of exosomal microRNAs in diseases.

Exosomes are an important group of extracellular vesicles that transfer several kinds of biomolecules and facilitate cell-cell communication. The content of exosomes, particularly the amounts of microRNA (miRNAs) inside these vesicles, demonstrates a disease-specific pattern reflecting pathogenic processes and may be employed as a diagnostic and prognostic marker. miRNAs may enter recipient cells through exosomes and generate a RISC complex that can cause degradation of the target mRNAs or block translation of their corresponding proteins. Therefore, exosome-derived miRNAs constitute an important mechanism of gene regulation in recipient cells. The miRNA content of exosomes can be used as an important tool in the detection of diverse disorders, particularly cancers. This research field has an important situation in cancer diagnosis. In addition, exosomal microRNAs offer a great deal of promise in the treatment of human disorders. However, there are still certain challenges to be resolved. The most important challenges are as follow: the detection of exosomal miRNAs should be standardized, exosomal miRNAs-associated studies should be conducted in large number of clinical samples, and experiment settings and detection criteria should be consistent across different labs. The goal of this article is to present an overview of the effects of exosome-derived microRNAs on a variety of diseases, including gastrointestinal, pulmonary, neurological, and cardiovascular diseases, with a particular emphasis on malignancies.

Detrimental effects of vitrification on integrin genes (α9 and ß1) and in vitro fertilization in mouse oocytes.

OBJECTIVE: Integrins are known as key molecules that importantly involve in fertilization. This study aimed to evaluate effects of vitrification on fertilization rate and expression of integrin genes, α9 and ß1, on mice oocytes in GV and MІІ stages. MATERIALS AND METHODS: From the ovarian tissue and fallopian tube of NMRI mice, germinal vesicle (GV, n = 200) and metaphase II (MII, n = 200) oocytes were obtained. Then, oocytes were distributed into 4 groups including non-vitrified GV, non-vitrified MII, vitrified GV, and vitrified MII. Cryotop method was used for vitrification and oocytes (for 4 weeks) were kept in liquid nitrogen. After that, by using an inverted microscope, the rate of survived oocytes was assessed. Also, in vitro fertilization (IVF) for oocytes, obtained from in vitro maturated MII and mice ovaries (ovulated MII), was done to assess embryos at differenced stages (2-cells, morula, and hatched). Finally, RT-qPCR was performed to investigate the mRNA expression of integrin genes (α9 and ß1). RESULTS: After vitrification, the rate of survived oocytes, 68.65%for GV and 65.07% % for MII, did not show a remarkable difference related to non-vitrified groups, while the fertilization rate in vitrified groups remarkably decrease compared to non-vitrified groups (p < 0.05). Also, the expression of α9 and ß1 genes was significantly altered in vitrified groups when compared to non-vitrified groups (p < 0.05). There was no significant difference in embryo developmental rates for non-vitrified and vitrified groups. CONCLUSION: Cryotop method for vitrification caused an alternation in oocyte quality by reducing fertilization rate and integrin gene expression.

The significance of N6-methyladenosine-modified non-coding RNAs in different disorders.

N6-methyladenosine (m6A) is the most widespread endogenous modification affecting the expression of eukaryotic mRNA transcripts. Recent studies have shown that the m6A marks within non-coding RNAs can affect their functions and expression in a manner similar to that of mRNA-coding genes. Since non-coding RNAs are involved in the pathophysiology of several disorders, identification of the role of m6A marks in the regulation of expression of non-coding RNAs can open a new era for identifying underlying mechanisms of several disorders and designing novel therapeutic modalities for a variety of disorders, particularly cancers. Moreover, a number of non-coding RNAs can affect m6A levels. In the current review, we discuss the impacts of m6A marks on the expression of non-coding RNAs in the context of different disorders, such as bone, gastrointestinal, neurologic, renal, pulmonary, hepatic and other disorders.

Interactions between non-coding RNAs and HIF-1α in the context of cancer.

Hypoxia-inducible factor 1α (HIF-1α) is a subunit of the HIF-1 transcription factor which is encoded by the HIF1A gene. This transcription factor is the main modulator of the cell response to hypoxia. Hypoxia-induced up-regulation of HIF-1α is involved in the pathogenesis of cancer. Recently, the interactions of several long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs) with HIF-1α have been reported. These ncRNAs regulate the expression of HIF-1α through different mechanisms. The regulatory roles of ncRNAs on HIF-1α are involved in the response of cancer cells to a wide range of anticancer drugs such as sorafenib, cisplatin, propofol, doxorubicin, and paclitaxel. Therefore, identification of the complex network between ncRNAs and HIF-1α not only facilitates the design of novel therapies but also promotes the efficacy of conventional anticancer treatments. This review aims to explain the interactions between these classes of ncRNAs and HIF-1α in the context of cancer.

Circular RNAs and inflammation: Epigenetic regulators with diagnostic role.

Circular RNAs (circRNAs) are a group of transcripts generally known to be non-coding transcripts, but occasionally producing short peptides. Circ_Ttc3/miR-148a, circ_TLK1/miR-106a-5p, circ_VMA21/miR-9-3p, circ_0068,888/miR-21-5p, circ_VMA21/miR-199a-5p, circ_AFF2/miR-375, circ_0008360/miR-135b-5p and circ-FBXW7/miR-216a-3p are examples of circRNA/miRNA pairs that contribute in the pathogenesis of immune-related conditions. CircRNAs have been found to regulate function of immune system and participate in the pathophysiology of immune-related disorders. In the current study, we searched PubMed and Google Scholar databases until July 2022 with the key words "circRNA" OR "circular RNA" AND "inflammation". Then, we assessed the abstract of retrieved articles to include original articles that assessed contribution of circRNAs in the pathoetiology of inflammation and related disorders. Finally, we went through the main texts of the articles and tabulated the available information. Therefore, the current study summarizes the role of circRNAs in the pathoetiology of sepsis, atherosclerosis, rheumatoid arthritis and osteoarthritis, immune-related cardiovascular, pulmonary, gastrointestinal and nervous system disorders.

Interplay between programmed death-ligand 1 and non-coding RNAs.

Programmed death-ligand 1 (PD-L1) is a transmembrane protein with essential roles in the suppression of adaptive immune responses. As an immune checkpoint molecule, PD-L1 can be exploited by cancer cells to evade the anti-tumor attacks initiated by the immune system. Thus, blockade of the PD1/PD-L1 axis can eliminate the suppressive signals and release the antitumor immune responses. Identification of the underlying mechanisms of modulation of the activity of the PD1/PD-L1 axis would facilitate the design of more efficacious therapeutic options and better assignment of patients for each option. Recent studies have confirmed the interactions between miRNAs/lncRNAs/circ-RNAs and the PD1/PD-L1 axis. In the current review, we give a summary of interactions between these transcripts and PD-L1 in the context of cancer. We also overview the consequences of these interactions in the determination of the response of patients to anti-cancer drugs.

NLRP3: Role in ischemia/reperfusion injuries.

NLR family pyrin domain containing 3 (NLRP3) is expressed in immune cells, especially in dendritic cells and macrophages and acts as a constituent of the inflammasome. This protein acts as a pattern recognition receptor identifying pathogen-associated molecular patterns. In addition to recognition of pathogen-associated molecular patterns, it recognizes damage-associated molecular patterns. Triggering of NLRP3 inflammasome by molecules ATP released from injured cells results in the activation of the inflammatory cytokines IL-1ß and IL-18. Abnormal activation of NLRP3 inflammasome has been demonstrated to stimulate inflammatory or metabolic diseases. Thus, NLRP3 is regarded as a proper target for decreasing activity of NLRP3 inflammasome. Recent studies have also shown abnormal activity of NLRP3 in ischemia/reperfusion (I/R) injuries. In the current review, we have focused on the role of this protein in I/R injuries in the gastrointestinal, neurovascular and cardiovascular systems.