Nicotinamide adenine dinucleotide kinase (NADK) is essential to the generation of nicotinamide adenine dinucleotide phosphate (NADP(H)), an important metabolic coupling factor involved in glucose-stimulated insulin secretion. In the present study, we showed that the expression of Nadk and Nadk2 transcripts and NADP(H) content were lower in islets of 80-week-old (aged) mice than those of 8-week-old (young) mice. This was associated with diminished oral glucose tolerance of old mice and the glucose-stimulated insulin secretion (GSIS) response of islets. Knockdown (KD) of Nadk or Nadk2 gene expression in NIT-1 cells impaired glucose-stimulated insulin secretion. Metabolomic analysis revealed that Nadk KD specifically affected purine metabolism in glucose-stimulated cells. The levels of 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) were higher in KD cells than in the non-targeting control (NTC) cells. Phosphorylation of AMP-activated protein kinase (AMPK) was elevated in glucose-treated KD cells compared to that of NTC cells. Increased AICAR level and AMPKα phosphorylation were observed in the glucose-stimulated islets of the aged mice. Genetic and pharmacological inhibition of AMPK promoted glucose-stimulated insulin release by KD cells and the aged mouse islets. It is likely that NADK is modulatory to AMPK activation in pancreatic β-cells and to their GSIS response. Enhanced AICAR formation in KD cells was accompanied by significantly increased conversion from inosine monophosphate (IMP) in a tetrahydrofolate (THF)-dependent manner. Folate supplementation augmented the GSIS response of KD cells and aged mouse islets. Taken together, these findings suggest that the aging-associated decline in NADK expression may underlie the reduced insulin secretory capacity of pancreatic β-cells.

Doxorubicin (DOX) is a potent anticancer drug; however, it is associated with significant cardiotoxicity. CDC20 is an E3 ubiquitin ligase that plays a role in cell cycle progression and apoptosis in various types of cancers. The involvement of CDC20 in DOX-induced cardiotoxicity (DIC) is poorly understood. Hence, this study aimed to explore the potential role of CDC20 in the development of DIC and assess whether CDC20 influences the antitumor effects of DOX.

Numerous chemicals are associated with carcinogenesis through epigenetic alterations in cells. To detect global epigenetic changes induced by carcinogens, the housekeeping gene can serve as a reporter locus, offering a baseline for identifying shifts in epigenetic marks. To investigate this potential, we developed a simple, cost-effective, and quantitative reporter system to assess chemically induced epigenetic effects, utilizing the thymidine kinase (TK) gene mutation assay as a foundation. Using a standard genotoxicity test cell line, human lymphoblast TK6, we edited the CpG promoter loci of the endogenous TK gene using the CRISPR/dCas9-SunTag-DNMT3A system. This epi-genotoxicity assay, employing modified mTK6 cells, provides a simple method for quantifying chemically induced epigenetic effects. The assay successfully detects both increased TK reversion rates induced by DNMT inhibitors, such as 5-Aza-2'-deoxycytidine and GSK-3484862, and, for the first time, a significant reduction in TK revertant frequency caused by the non-genotoxic carcinogen 12-O-tetradecanoylphorbol-13-acetate (TPA). Chromatin immunoprecipitation and western blotting analyses revealed that TPA treatment led to a global decrease in H3K27Ac levels, likely driven by TPA-mediated inflammation. These results demonstrate the utility of the epi-genotoxicity assay as a valuable tool for evaluating dual-directional epigenetic changes triggered by chemical exposure.

Salmonella enterica is a clinically significant oro-fecal pathogen that causes a wide variety of illnesses and can lead to epidemics. S. enterica expresses a lot of virulence factors that enhance its pathogenesis in host. For instance, S. enterica employs a type three secretion system (T3SS) to translocate a wide array of effector proteins that could change the surrounding niche ensuring suitable conditions for the thrive of Salmonella infection. Many antimicrobials have been recently introduced to overcome the annoying bacterial resistance to antibiotics. Enoxacin is member of the second-generation quinolones that possesses a considerable activity against S. enterica. The present study aimed to evaluate the effect of enoxacin at sub-minimum inhibitory concentration (sub-MIC) on S. enterica virulence capability and pathogenesis in host. Enoxacin at sub-MIC significantly diminished both Salmonella invasion and intracellular replication within the host cells. The observed inhibitory effect of enoxacin on S. enterica internalization could be attributed to its ability to interfere with translocation of the T3SS effector proteins. These results were further confirmed by the finding that enoxacin at sub-MIC down-regulated the expression of the genes encoding for T3SS-type II (T3SS-II). Moreover, enoxacin at sub-MIC lessened bacterial adhesion to abiotic surface and biofilm formation which indicates a potential anti-virulence activity. Importantly, in vivo results showed a significant ability of enoxacin to protect mice against S. enterica infection and decreased bacterial colonization within animal tissues. In nutshell, current findings shed light on an additional mechanism of enoxacin at sub-MIC by interfering with Salmonella intracellular replication. The outcomes presented herein could be further invested in conquering bacterial resistance and open the door for additional effective clinical applications.

Lymphomas are complex malignancies of blood cells, characterized by the malignant transformation of lymphocytes. This transformation is partially driven by disruptions in epigenetic regulation, particularly the acetylation of histones. Among the key players in this process are histone deacetylases (HDACs), whose aberrant activity contributes significantly to lymphoma development. Consequently, targeting HDACs represents a promising pharmacotherapeutic approach. Several HDAC inhibitors (HDACis) have demonstrated significant anticancer effects, with four FDA-approved molecules-vorinostat, romidepsin, belinostat, and panobinostat-forming critical components of chemotherapy regimens for lymphoma treatment. These HDAC inhibitors exhibit their therapeutic efficacy through mechanisms that indirectly impact cellular memory and induce cancer cell death via apoptosis and cell cycle arrest. Their clinical effectiveness is particularly notable in various types of lymphomas, underscoring their therapeutic potential. The objective of this review is to provide a detailed analysis of FDA-approved HDACis, focusing on their molecular mechanisms of action and clinical applications in lymphoma treatment. Specifically, we aim to elucidate how these inhibitors modulate epigenetic regulation to achieve therapeutic efficacy, highlight their utility across different lymphoma subtypes, and examine their integration into combination therapies with other anticancer agents. Furthermore, this review seeks to identify gaps in current knowledge and propose directions for future research, including the development of next-generation HDAC inhibitors and strategies for optimizing their clinical use. By consolidating existing evidence, we strive to enhance the understanding of HDACis' role in lymphoma therapy and inspire advancements in their therapeutic potential.

This study aimed to explore the potential correlation between the metabolic intermediate L-2-hydroxyglutarate (L-2-HG) and T cell exhaustion, as well as the underlying mechanisms involved. In this study, we investigated the presence of exhausted T (Tex) cells in patients under certain conditions: HIV infection, chronic leukemia, and hepatocellular carcinoma. To gain insights into the epigenetic signatures and transcriptome changes in Tex cells, we employed a combination of RNA-seq and ATAC-seq analyses. To evaluate the impact of L-2-HG on mitochondrial function, differentiation, and antitumor capacity of Tex cells, we utilized in vitro cell culture experiments and animal tumor models. We observed mitochondrial depolarization and metabolic dysfunction in Tex cells, accompanied by a significant reduction in L-2-HG levels. Moreover, altered epigenetic characteristics were observed in Tex cells, including a substantial increase in H3K27me3 abundance. Culturing Tex cells with L-2-HG demonstrated improved mitochondrial metabolism, reduced H3K27me3 abundance, and enhanced memory T cell differentiation. In a mouse melanoma tumor model, L-2-HG-treated CD8+ T cells for adoptive therapy led to significantly reduced tumor volume and significantly enhanced effector function of T cells. The study revealed that L-2-HG acted as an immune metabolite through epigenetic modifications of Tex cells.

Biostimulants help plants to cope with abiotic stresses and using those obtained by recycling waste bioproducts is an eco-friendly technology with great potential. Quinoa (Chenopodium quinoa Willd.) is a highly nutritious grain originally cultivated in the Andes but now spreading worldwide. Before consumption, quinoa seeds undergo a dehulling process that produces large amounts of a waste product rich in saponins and other bioactive compounds. In this study, the by-product of quinoa seed dehulling (quinoa hull powder, QHP) was analysed for its plant biostimulant activity. The objective was to analyze whether QHP could improve growth and induce biochemical and transcriptional changes under control or saline (25, 50, and 100 mM NaCl) conditions in the model plant Arabidopsis thaliana. QHP was supplied either by pre-soaking seeds prior to sowing (seed priming) or added to the seedling growth medium. Complete and partial recovery of germinability to control levels was observed in seeds primed with 0.05 mg mL-1 QHP in the presence of 50 and 100 mM NaCl, respectively. Seedlings transferred to QHP-supplemented saline medium showed improved shoot and root biomass and primary root length as well as reduced oxidative stress (MDA, and H2O2 production). RT-qPCR analysis of stress-responsive genes revealed that some were induced by QHP alone while salt-induced expression of others was modulated by QHP. The phytochemical composition of QHP suggests that, in addition to saponins, protective compounds, such as proline, spermidine, carotenoids, and polyphenols, could be potentially responsible for its activity.

Aromatic ring-hydroxylating dioxygenases (ARHDs) play a crucial role in the aerobic biodegradation of both natural and anthropogenic aromatic compounds. Although their ability to process contaminants is not entirely understood, it is thought to have evolved from the transformation of structurally similar secondary plant metabolites (SPMs). Hence, to investigate this connection, we tested a variety of SPMs from the monoterpene and flavonoid classes as carbon sources and transcriptional effectors of several phylogenetically distant ARHD genes involved in the degradation of aromatic pollutants. Specifically, we focused on bphA1, nahA1 and phtA1 in Rhodococcus opacus C1, whose genomic analysis is also presented hereinafter, and bphA1a, nahA1-bphA1b and etbA1ab in Rhodococcus sp. WAY2. Whilst induction was only observed with (R)-carvone for bphA1a and nahA1-bphA1b of strain WAY2, and with p-cymene for nahA1 and nahA1-bphA1b of strains C1 and WAY2, respectively, an extensive inhibition by flavonoids was observed for most of the genes in both strains. To the best of our knowledge, our study is the first to report the effect of flavonoids and monoterpenes on the transcription of nahA1, etbA1 and phtA1 genes. In addition, we show that, in contrast to pseudomonads, many flavonoids inhibit the transcription of the ARHD genes in rhodococci. Thus, our work provides a new perspective on flavonoids as the transcriptional effectors of ARHDs, highlighting the significant variability of these enzymes and the divergent responses that they elicit. Moreover, our results contribute to understanding the complex interactions between microorganisms and SPMs and provide insights into the molecular basis of a number of them.

Adjuvants are crucial in vaccines and cancer therapies, enhancing therapeutic efficacy through diverse mechanisms. In vaccines, adjuvants are traditionally valued for amplifying immune responses, ensuring robust and long-lasting protection against pathogens. In cancer treatments, adjuvants can boost the effectiveness of chemotherapy or immunotherapy by targeting tumor antigens, rendering cancer cells more vulnerable to treatment. Recent research has uncovered new molecular-level effects of the adjuvants, mainly through epigenetic mechanisms. Epigenetics encompasses heritable modifications in gene expression that do not alter the DNA sequence, impacting processes such as DNA methylation, histone modification, and non-coding RNA expression. These epigenetic changes play a pivotal role in regulating gene activity, influencing immune pathways, and modulating the strength and duration of immune responses. Whether in vaccines or cancer treatments, understanding how adjuvants interact with epigenetic regulators offers significant potential for developing more precise, cell-targeted therapies across various medical fields. This review delves into the evolving role of adjuvants and their interactions with epigenetic mechanisms. It also examines the potential of harnessing epigenetic changes to enhance adjuvant efficacy and explores the novel use of epigenetic inhibitors as adjuvants in therapeutic settings.

Embigin (EMB) is a transmembrane glycoprotein highly expressed in glioblastoma multiforme (GBM), yet its role in GBM progression remains unclear. In this study, we investigate the function of intracellular EMB in promoting GBM progression and evaluate the effect of Ganxintriol A, a traditional Chinese herbal extract, in GBM treatment.

The chronic illness known as oral submucous fibrosis (OSF) results in tissue fibrosis, precancerous lesions, and scarring. It usually manifests itself in the buccal mucosa. It frequently occurs in the buccal mucosa. Von Hippel-Lindau (VHL) is an essential component of E3 ubiquitin ligase complex. The loss of VHL led to reduced fibrotic responses, accompanied by ameliorated fiber deposition. However, the precise impact of VHL on OSF is yet unclear. OSF tissues and normal mucosal tissues were applied to analyze the distinct expression of VHL and histone deacetylase 6 (HDAC6). Oral fibroblasts were treated to arecoline to simulate OSF in vitro, and molecular biological experiments were conducted to identify the role of VHL in buccal mucosa fibroblasts (BMFs). VHL was downregulated and HDAC6 was upregulated in OSF tissues and BMFs. Overexpression of VHL inhibited fibrosis in arecoline-treated BMFs. VHL inhibits the level of HDAC6 by inducing the ubiquitination of HDAC6. Knockdown of HDAC6 reduces the fibrogenic ability of BMFs. Furthermore, overexpression of HDAC6 contributes to the activation of NF-κB signaling in BMFs. HDAC6 selective inhibitor ACY-1215 inhibited the NF-κB signaling pathway. VHL attenuated arecoline-induced OSF by inhibiting the ubiquitination of HDAC6 and blocking NF-κB pathway. As a result, our study offers new perspectives into the discovery of novel tactics that can be employed against OSF.

The formation of biofilm by foodborne pathogens increases the risk of foodborne diseases, resulting in major health risks. Research on strategies for eliminating biofilm formation by foodborne pathogens is urgently needed. Therefore, the objective of this study was to construct a new technique for controlling foodborne bacteria and inhibiting the biosynthesis of biofilm via using natural products. The essential orange oil (EOO) and cell-free filtrate of Lactobacillus pentosus RS2 were used as antibacterial and antibiofilm agents against B. cereus RS1, the strongest biofilm-forming strain. The mixture of cell-free filtrate (CFF) and EOO (CFF/EOO) was the best antibiofilm agent under all tested conditions. The minimal inhibitory concentration (MIC) test revealed that 400 μl ml-1 CFF and 16 μl ml-1 EOO completely inhibited the growth of B. cereus. The treatment of three commercial surfaces with CFF/EOO resulted in a high reduction in biofilm synthesis, with adhesion percentages of 33.3, 36.3, and 40.8% on stainless steel, aluminum foil, and aluminum, respectively. The aluminum surface had the greatest adhesion with B. cereus RS1 among the three tested surfaces. These results were confirmed by expression analysis of three essential coding genes, sinR, calY, and spo0A, participating in biofilm formation in B. cereus. The biofilm-negative regulator gene sinR was overexpressed, whereas the biofilm-positive regulator genes calY and spo0A were down-expressed in B. cereus RS1 after treatment with antibiofilm agents, compared with those in the untreated sample. This study revealed that CFF/EOO was more effective at activating sinR (2.099 ± 0.167-fold increase) and suppressing calY and spo0A (0.314 ± 0.058 and0.238 ± 0.04-fold decrease, respectively) compared to control. This result confirmed the biochemical estimation of biofilm formation in B. cereus after treatment with all the experimental agents. The EOO and CFF of L. pentosus RS2 can be used as strong antibacterial and antibiofilm agents against foodborne bacteria. These products reduced the biofilm formation on trade surfaces affecting the expression of three essential biofilm regulatory genes. This study considered novel research concerning the potential antibiofilm activity of EOO combined with CFF of L. pentosus and the molecular analysis of genes regulating biofilm production under stress of CFF/EOO.

Environmental factors play an important role in anthocyanin biosynthesis, and potassium, an essential nutrient for blueberry growth, can act as an enzyme activator. However, few reports exist on the transcriptional and anthocyanin metabolic changes in blueberries regulated by potassium. The results indicated that potassium treatment significantly increased the contents of malvidin, petunidin, and delphinidin in blueberry fruits and accelerated early color development, particularly favoring the accumulation of darker pigments such as malvidin, petunidin, and delphinidin when applied at the young fruit stage. Transcriptome analysis identified 102 glucose metabolism-related genes and 12 differential potassium transport genes potentially involved in potassium-mediated anthocyanin synthesis and accumulation, with AKT1 and KUP potassium transporters being upregulated under potassium fertilization. In the anthocyanin biosynthesis pathway, 13 genes, including UFGT, F3H, CHI, HCT, C12RT1, DFR, and F3'5'H, were closely linked to flavonoid and anthocyanin metabolite synthesis regulated by potassium. Furthermore, potassium treatment markedly enhanced the activities of key enzymes, F3H, F3'5'H, and UFGT, in the anthocyanin synthesis pathway of blueberry fruits. Overall, these findings elucidate the influence of potassium application timing on anthocyanin synthesis and provide valuable insights into the molecular mechanisms governing anthocyanin biosynthesis in blueberries.

Carbon dots, are now considered safe, environment-friendly materials. Spermidine carbon dots (Spd-CDs) have been used as new agrochemicals for abiotic stress, but in-depth studies of salt stress remain scarce. Here, foliar application of Spd-CDs improved salt stress tolerance in tomatoes, and the beneficial effects were concentration-dependent. Tomato seedlings supplied with Spd-CDs (3.0 mg/L) had a greater height, a higher maximum quantum yield of PSII, and a higher net photosynthetic rate than controls after being exposed to 120 mM NaCl for 7 d. Molecular evidence showed that Spd-CDs promoted H2O2 molecule production by inducing the expression of respiratory burst oxidase homolog 1 (rboh1) and polyamine oxidase 5 (pao5), thus causing H2O2 molecule production and conferring resistance to salt stress. The role of RBOH1- and PAO5-dependent H2O2 molecule generation was evaluated by manipulating endogenous H2O2 levels and in rboh1 and pao5 mutants. Spd-CDs-meditated H2O2 regulation of salt tolerance could be articulated by reducing iron deficiency, maintaining ion homeostasis, and reducing root-to-shoot Na+ loading. Overall, the ROS signal molecule produced by RBOH1 and PAO5 protein was involved in the control of salt tolerance by Spd-CDs. These findings demonstrate that Spd-CDs are an effective and durable strategy to improve plant performance under salt stress, and to increase food security and quality.

Although bacterial cells typically contain a single chromosome, some species are naturally polyploid and carry multiple copies of their chromosome. Polyploid chromosomes can be identical or heterogeneous, the latter giving rise to bacterial heterozygosity. Although the benefits of heterozygosity are well studied in eukaryotes, its consequences in bacteria are less understood. Here, we examine this question in the context of antibiotic resistance to understand how bacterial genomic heterozygosity affects bacterial survival. Using a cell-wall-deficient model system in the actinomycete Kitasatospora viridifaciens, we found that heterozygous cells that contain different chromosomes expressing different antibiotic resistance markers persist across a broad range of antibiotic concentrations. Recombinant cells containing the same resistance genes on a single chromosome also survive these conditions, but these cells pay a significant fitness cost due to the constitutive expression of these genes. By contrast, heterozygous cells can mitigate these costs by flexibly adjusting the ratio of their different chromosomes, thereby allowing rapid responses in temporally and spatially variable environments. Our results provide evidence that bacterial heterozygosity can increase adaptive plasticity in bacterial cells in a similar manner to the evolutionary benefits provided by multicopy plasmids in bacteria.

The current study evaluated the effects of dietary supplementation of Triphala (TR) on yellow perch (Perca flavescens) growth performance, immune response, related gene expression, and intestinal histological structure. The experimental design included four groups: one control group (0% TR/ kg diet) and three TR-supplemented groups with 2, 4, and 6%/kg diet for four weeks and each group was allocated in triplicates with 30 fish each. Sampling included three fish from each replicate for evaluating immune response and gene expression. Findings showed that Triphala markedly improved growth performance, Immunoglobulin M (IgM) levels, lysozyme activity, and Nitric Oxide (NO) activity with the most significant (p < 0.05) results for 6% TR/kg diet group. The TR groups also showed significantly decreased glucose and cortisol concentrations with the lowest values for the 6% TR/kg diet group. Moreover, TR-incorporated groups revealed significantly upregulated expression (p < 0.05) of growth [Insulin-Like Growth Factor-1 (IGF-1)] and immune [Alpha 2 Macroglobulin (A2M), Serum Amyloid A (SAA) and Complement Component C3 (CCC3)] genes in incorporated groups, specially the 6% TR group. Moreover, the intestinal morphometric histological analysis revealed that villus length was increased in a dose-dependent manner, coping with other enhanced parameters. Current results endorse the positive effects of Triphala incorporation on yellow perch farming as a safe alternative option to enhance growth performance, immune response, related gene expression, and intestinal histology.

Osimertinib, a third-generation EGFR-tyrosine kinase inhibitor, is the first-line therapy for lung cancer harboring EGFR mutations. The mechanisms underlying osimertinib resistance are diverse, with approximately half remaining unknown. Epigenetic dysregulation is implicated in drug resistance; however, the mechanisms remain unclear. Therefore, we investigated epigenetic involvement in osimertinib resistance and its therapeutic potential. We established osimertinib-resistant cells and used an assay for transposase-accessible chromatin using sequencing to evaluate chromatin accessibility, finding significant changes post-resistance. Combining the assay for transposase-accessible chromatin and RNA sequencing data, we identified FGF1 as a resistance-related gene regulated by histone modifications. FGF1 induced osimertinib resistance, and its suppression attenuated resistance. Bromodomain and extra-terminal domain inhibitors combined with osimertinib overcame osimertinib resistance by reducing FGF1 expression. Increased FGF1 expression was observed in osimertinib-resistant clinical samples. This combination therapy was effective in cell lines and mouse xenograft models. These results suggest targeting histone modifications using bromodomain and extra-terminal domain inhibitors as a novel approach to overcoming osimertinib resistance.

Inflammatory bowel disease (IBD) encompasses chronic inflammation of the colon and rectum, posing significant health challenges. Previous studies have shown potential therapeutic effects of natural compounds on IBD. Chrysin, a naturally occurring flavonoid, has been suggested to modulate inflammatory pathways and gut microbiota, but its comprehensive impact on ulcerative colitis remains inadequately explored.

Doxorubicin (DOX)-associated cardiotoxicity is characterized by long-term manifestations, whose mechanisms remain incompletely understood, and is exacerbated by various risk factors, with age being a prominent contributor. The objective of this study was to assess the enduring cardiac molecular impacts of DOX in old CD-1 male mice, focusing on ubiquitinated proteins. At 19 months of age, DOX group received a cumulative dose of 9.0 mg/kg of DOX, while control animals got saline solution. Animals were sacrificed 2 months after the administration. DOX induced heart structural changes and increased proteolytic activity. Additionally, increased protein ubiquitination was observed in DOX group, despite the decreased content of the E3 ubiquitin-protein ligase Atrogin-1. A search of poly-ubiquitinated proteins, enriched by tandem ubiquitin-binding entities (TUBEs), showed increased poly-ubiquitination of proteins associated with sarcomere organization and mitochondrial metabolism processes by DOX. Increased mitochondrial density inferred by higher citrate synthase activity was found in DOX group. Moreover, decreased biogenesis and auto(mito)phagy occurred in DOX animals, proven by decreased peroxisome proliferator-activated receptor γ coactivator 1 α, Beclin1 and microtubule-associated protein light chain 3 content. These findings indicate a reduction in mitochondrial biogenesis and accumulation of dysfunctional mitochondria in the aged heart, along with elevated levels of poly-ubiquitinated proteins after DOX treatment. Thus, the disruption of mitochondrial remodeling and impaired protein ubiquitination emerge as enduring consequences of DOX-induced cardiotoxicity, persisting for even 2 months after DOX exposure. This underscores the long-lasting impact of DOX, with significant effects continuing beyond the period of administration, which advocates for longer clinical surveillance.

Skeletal muscle is the most abundant tissue in the human body and is responsible for movement, metabolism, energy production and longevity. Muscle atrophy is a frequent complication of several diseases and occurs when protein degradation exceeds protein synthesis. Genetics, ageing, nerve injury, weightlessness, cancer, chronic diseases, the accumulation of metabolic byproducts and other stimuli can lead to muscle atrophy. Muscular dystrophy is a neuromuscular disorder, part of which is caused by the deficiency of dystrophin protein and is mostly related to genetics. Muscle atrophy and muscular dystrophy are accompanied by dynamic changes in transcriptomic, translational and epigenetic regulation. Multiple signalling pathways, such as the transforming growth factor-β (TGF-β) signalling pathway, the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) pathway, inflammatory signalling pathways, neuromechanical signalling pathways, endoplasmic reticulum stress and glucocorticoids signalling pathways, regulate muscle atrophy. A large number of long noncoding RNAs (lncRNAs) have been found to be abnormally expressed in atrophic muscles and dystrophic muscles and regulate the balance of muscle protein synthesis and degradation or dystrophin protein expression. These lncRNAs may serve as potential targets for treating muscle atrophy and muscular dystrophy. In this review, we summarized the known lncRNAs related to muscular dystrophy and muscle atrophy induced by denervation, ageing, weightlessness, cachexia and abnormal myogenesis, along with their molecular mechanisms. Finally, we explored the potential of using these lncRNAs as therapeutic targets for muscle atrophy and muscular dystrophy, including the methods of discovery and clinical application prospects for functional lncRNAs.