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The DNA damage response (DDR) and cellular metabolism exhibit a complex, bidirectional relationship crucial for maintaining genomic integrity. Studies across multiple organisms, from yeast to humans, have revealed how cells rewire their metabolism in response to DNA damage, supporting repair processes and cellular homeostasis. We discuss immediate metabolic shifts upon damage detection and long-term reprogramming for sustained genomic stability, highlighting key signaling pathways and participating molecules. Importantly, we examine how DNA repair processes can conversely induce metabolic changes and oxidative stress through specific mechanisms, including the histone H2A variant X (H2AX)/ataxia telangiectasia mutated (ATM)/NADPH oxidase 1 (Nox1) pathway and repair-specific ROS signatures. The review covers organelle-specific responses and metabolic adaptations associated with different DNA repair mechanisms, with a primary focus on human cells. We explore the implications of this DDR–metabolism crosstalk in cancer, aging, and neurodegenerative diseases, and discuss emerging therapeutic opportunities. By integrating recent findings, this review provides a comprehensive overview of the intricate interplay between DDR and cellular metabolism, offering new perspectives on cellular resilience and potential avenues for therapeutic intervention.

Background Sterol carrier protein 2 (SCP2) plays a critical role in intracellular lipid transport and metabolism across human tissues. The objective of this study was to perform a comprehensive pan-cancer analysis of SCP2, evaluating its expression, prognostic significance, and functional mechanisms. Methods We analyzed SCP2 expression using data from TCGA and GTEx databases. Prognostic significance was evaluated via Kaplan-Meier and Cox regression analyses, alongside nomogram construction. Functional mechanisms were investigated through GO, KEGG, and GSEA enrichment analyses. Genetic alterations, DNA methylation, single-cell functions, and immune infiltration were assessed using multiple bioinformatic platforms. The effects of SCP2 on cancer cell proliferation, migration, apoptosis, and sensitivity to ferroptosis were verified by in vitro experiments. Results SCP2 was differentially expressed in multiple tumors and correlated with clinical outcomes and immune infiltration. Enrichment analyses linked SCP2 to lipid metabolism-related pathways. In colon adenocarcinoma (COAD), SCP2 was downregulated and functioned as a tumor suppressor, as its overexpression inhibited proliferation and migration, promoted apoptosis, and strongly enhanced ferroptosis sensitivity in colon cancer cells. Conclusion Our pan-cancer analysis highlights the broad biological and clinical significance of SCP2. It functions as a tumor suppressor and key regulator of ferroptosis in COAD, highlighting its potential as a promising therapeutic target.

Seaweed fertilizer, formulated primarily with seaweed extract as its main ingredient, has been extensively studied and found to significantly improve nutrient use efficiency, increase crop yield and quality, and enhance soil properties under field conditions. This growing body of evidence shows that seaweed fertilizer is a suitable option for sustainable agriculture in China. However, a comprehensive and quantitative analysis of the overall effects of seaweed fertilizer application in China is lacking. To address this gap, we conducted a meta-analysis of relevant studies on the effects of seaweed fertilizers under field conditions in China with MetaWin and SPSS software. Our analysis examined the effects of seaweed fertilizers on crop yield, quality, and growth under different preparation methods, application techniques, and regions. Our results showed that the application of seaweed fertilizer led to a significant average increase in crop yield of 15.17% compared with the control treatments. Root & tuber crops exhibited the most pronounced response, with a yield boost of 21.19%. Moreover, seaweed fertilizer application significantly improved crop quality, with elevations in the sugar-acid ratio (38.32%) vitamin C (18.07%), starch (19.65%), and protein (11.45%). In addition, plant growth parameters such as height, stem thickness, root weight, and leaf area showed significant enhancement with seaweed fertilizer use. The yield-increasing effect of seaweed fertilizers varied depending on their preparation and use method, climate, and soil of application location. Our study provides fundamental reference data for the efficient and scientific application of seaweed fertilizers in agricultural practices.

Stem cells play critical roles both in the development of cancer and therapy resistance. Although mesenchymal stem cells (MSCs) can actively migrate to tumor sites, their impact on chimeric antigen receptor modified T cell (CAR-T) immunotherapy has been little addressed. Using an in vitro cell co-culture model including lymphoma cells and macrophages, here we report that CAR-T cell-mediated cytotoxicity was significantly inhibited in the presence of MSCs. MSCs caused an increase of CD4 + T cells and Treg cells but a decrease of CD8 + T cells. In addition, MSCs stimulated the expression of indoleamine 2,3-dioxygenase and programmed cell death-ligand 1 which contributes to the immune-suppressive function of tumors. Moreover, MSCs suppressed key components of the NLRP3 inflammasome by modulating mitochondrial reactive oxygen species release. Interestingly, all these suppressive events hindering CAR-T efficacy could be abrogated if the stanniocalcin-1 (STC1) gene, which encodes the glycoprotein hormone STC-1, was knockdown in MSC. Using xenograft mice, we confirmed that CAR-T function could also be inhibited by MSC in vivo, and STC1 played a critical role. These data revealed a novel function of MSC and STC-1 in suppressing CAR-T efficacy, which should be considered in cancer therapy and may also have potential applications in controlling the toxicity arising from the excessive immune response. Immunotherapy is a type of cancer treatment that helps the immune system fight cancer. For example, chimeric antigen receptor T cell (CAR-T) therapy is used to target several types of blood cancer. It works by reprogramming patients’ immune cells to target specific tumor cells. In blood cancers, CAR-T therapy works very well, but it can cause extreme responses from the patient’s immune system, which can be life threatening. In solid tumors, CAR-T therapy is much less successful because the tumors secrete molecules into the space surrounding them, which weaken the immune processes that attack cancerous cells. Stem cells are the master cells of the body. Originating in the bone marrow, they can repair and regenerate the body’s cells. Cancer stem cells play a role in resistance to CAR-T therapy, due – in part – to their ability to renew themselves, but the role of another type of stem cell, called mesenchymal stem cells, was less clear. Mesenchymal stem cells develop into tissues that line organs and blood vessels. Although it is known that mesenchymal stem cells are present in most cancers and play a role in shaping and influencing the space around tumors, their impact on CAR-T therapy has not been studied in depth. To find out more, Zhang et al. looked at the influence of a protein, called staniocalcin-1 (STC1), on CAR-T therapy, by studying cells grown in the laboratory and human tumor cells that had been implanted in mice. Zhang et al. found that mesenchymal stem cells reduce the ability of CAR-T therapy to destroy cancer cells and that they needed STC1 to do this successfully. They also increased the expression of molecules that dampen the immune system, and suppressed molecules called inflammasomes, which are an important part of the way the immune system detects disease. Moreover, reducing the amount of STC1 that mesenchymal stem cells expressed restored the effectivity of CAR-T therapy. This study increases our understanding of the way that mesenchymal stem cells affect CAR-T therapy. It has the potential to open up a new way of improving the efficiency of this treatment and of reducing the harmful side effects that it can cause.

Soy sauce aroma type baijiu (also known as Maotai-flavor baijiu) is one of the most popular types of baijiu in China. Traditionally, it is mainly produced in Southwest China. However, in recent decades, some other regions in China have also been able to produce high-quality soy sauce aroma type baijiu, but their microbial flora characteristics during fermentation are still unclear. Here, the bacterial microbial community structure of fermented grains in different rounds of Lutaichun soy sauce aroma type baijiu produced in North China was studied by high-throughput sequencing technology, and the potential probiotics strains with good characteristics (alcohol tolerance, etc.) were screened. The results showed that lactic acid bacteria were the main bacteria in the process of baijiu fermentation. However, as the number of repeated fermentation rounds increased, the proportion of lactic acid bacteria decreased. Firmicutes (96.81%) were the main bacteria in baijiu fermentation at the phylum level, and Lactobacillus (66.50%) were the main bacteria at the genus level. Finally, two strains with high resistance to alcohol stress, Lactiplantibacillus plantarum LTJ12 and Pediococcus acidilactici LTJ28, were screened from 48 strains of lactic acid bacteria in the fermented grains. The survival rates of L. plantarum LTJ12 and P. acidilactici LTJ28 under the 8% alcohol stress treatment were 59.01% and 55.50%, respectively. To the best of our knowledge, this study is the first to reveal the microbial succession of fermented grains in different rounds of soy sauce aroma type baijiu from North China, and has the benefit of explaining the deep molecular mechanism in the process of baijiu fermentation. In addition, the obtained lactic acid bacteria strains with high alcohol tolerance could be conducive to the development of new products such as active probiotic alcoholic beverages and may have important industrial development prospects also.

Background Pulsed transcranial ultrasound stimulation (pTUS) can modulate the neuronal activity of motor cortex and elicit muscle contractions. Cortico-muscular coupling (CMC) can serve as a tool to identify interaction between the oscillatory activity of the motor cortex and effector muscle. This research aims to explore the neuromodulatory effect of low-intensity, pTUS with different number of tone burst to neural circuit of motor-control system by analyzing the coupling relationship between motor cortex and tail muscle in mouse. The motor cortex of mice was stimulated by pulsed transcranial ultrasound with different number of tone bursts (NTB = 100 150 200 250 300). The local field potentials (LFPs) in tail motor cortex and electromyography (EMG) in tail muscles were recorded simultaneously during pTUS. The change of integral coupling strength between cortex and muscle was evaluated by mutual information (MI). The directional information interaction between them were analyzed by transfer entropy (TE). Results Almost all of the MI and TE values were significantly increased by pTUS. The results of MI showed that the CMC was significantly enhanced with the increase of NTB. The TE results showed the coupling strength of CMC in descending direction (from LFPs to EMG) was significantly higher than that in ascending direction (from EMG to LFPs) after stimulation. Furthermore, compared to NTB = 100, the CMC in ascending direction were significantly enhanced when NTB = 250, 300, and CMC in descending direction were significantly enhanced when NTB = 200, 250, 300. Conclusion These results confirm that the CMC between motor cortex and the tail muscles in mouse could be altered by pTUS. And by increasing the NTB (i.e. sonication duration), the coupling strength within the cortico-muscular circuit could be increased, which might further influence the motor function of mice. It demonstrates that, using MI and TE method, the CMC could be used for quantitatively evaluating the effect of pTUS with different NTBs, which might provide a new insight into the effect of pTUS neuromodulation in motor cortex.

Upon vascular injury, vascular smooth muscle cells (VSMCs) change from a contractile phenotype to a synthetic phenotype, thereby leading to atherogenesis and arterial restenosis. Myocardin (MYOCD) is essential for maintaining the contractile phenotype of VSMCs. Deletion of MYOCD in VSMCs triggers autophagy. However, the molecular mechanism underlying the effect of MYOCD on autophagy is not clear. In this study, knockdown of MYOCD in human aortic VSMCs (HA-VSMCs) triggered autophagy and diminished the expression of SMC contractile proteins. Inhibition of autophagy in MYOCD-knockdown cells restored the expression of contractile proteins. MYOCD activated the transcription of miR-30a by binding to the CArG box present in its promoter, as confirmed by luciferase reporter and chromatin immune coprecipitation assays, while miR-30a decreased the expression of autophagy protein-6 (ATG6, also known as beclin1) by targeting its 3′UTR. Restoring the expression of miR-30a in MYOCD-knockdown cells upregulated the levels of contractile proteins. Treatment of VSMCs with platelet-derived growth factor type BB (PDGF-BB) resulted in the transformation of VSMCs to a proliferative phenotype. A low level of miR-30a was observed in PDGF-BB-treated HA-VSMCs, and re-expression of miR-30a led to a decrease in proliferative marker expression. Furthermore, using a wire injury mouse model, we found that miR-30a expression was significantly downregulated in the arterial tissues of mice and that restoration of miR-30a expression at the injured site abolished neointimal formation. Herein, MYOCD could inhibit autophagy by activating the transcription of miR-30a and that miR-30a-mediated autophagy defects could inhibit intimal hyperplasia in a carotid arterial injury model.

Anaplasmosis is a highly prevalent tick-borne intracellular bacterial disease that affects various host species globally, particularly ruminants in tropical and subtropical regions. However, information regarding the distribution and epidemiology of anaplasmosis in small and large ruminants on Hainan Isalnd is limited. To address this knowledge gap, the present study aimed to assess the occurrence of Anaplasma spp. infections in goats ( N  = 731) and cattle ( N  = 176) blood samples using nested PCR and conventional PCR based assays. The results revealed an overall prevalence of 30.1% in goats and 14.8% in cattle. The infection rates of A. bovis , A. phagocytophilum , A. ovis and A. capra in goat samples were 22.7%, 13.8%, 2.0% and 3.4%, respectively, while the infection rates of A. bovis , A. phagocytophilum and A. marginale in cattle samples were 11.4%, 6.3% and 5.7%, respectively. A. bovis exhibited the highest prevalence among the Anaplasma spp. in both goat and cattle samples. In addition, the most frequent co-infection was the one with A. phagocytophilum and A. bovis. It was found that the age, sex and feeding habits of cattle and goats were considered to be important risk factors. Evaluation of the risk factor relating to the rearing system showed that the infection rate for the free-range goats and cattle was significantly higher when compared with stall-feeding system. This study represents one of the largest investigations on the distribution, prevalence, and risk factors associated with Anaplasma infection in ruminants on Hainan Island, highlighting a higher circulation of the infection in the region than previously anticipated. Further reasesrch is necessary to investigate tick vectors, reservoir animals, and the zoonotic potential of the Anaplasma spp. in this endemic region of Hainan Island.

Background Fine tactile sensation plays an important role in motor relearning after stroke. However, little is known about its dynamics in post-stroke recovery, principally due to a lack of effective evaluation on neural responses to fine tactile stimulation. This study investigated the post-stroke alteration of cortical connectivity and its functional structure in response to fine tactile stimulation via textile fabrics by electroencephalogram (EEG)-derived functional connectivity and graph theory analyses. Method Whole brain EEG was recorded from 64 scalp channels in 8 participants with chronic stroke and 8 unimpaired controls before and during the skin of the unilateral forearm contacted with a piece of cotton fabric. Functional connectivity (FC) was then estimated using EEG coherence. The fabric stimulation induced FC (SFC) was analyzed by a cluster-based permutation test for the FC in baseline and fabric stimulation. The functional structure of connectivity alteration in the brain was also investigated by assessing the multiscale topological properties of functional brain networks according to the graph theory. Results In the SFC distribution, an altered hemispheric lateralization (HL) (HL degree, 14%) was observed when stimulating the affected forearm in the stroke group, compared to stimulation of the unaffected forearm of the stroke group (HL degree, 53%) and those of the control group (HL degrees, 92% for the left and 69% for the dominant right limb). The involvement of additional brain regions, i.e., the distributed attention networks, was also observed when stimulating either limb of the stroke group compared with those of the control. Significantly increased (P < 0.05) global and local efficiencies were found when stimulating the affected forearm compared to the unaffected forearm. A significantly increased (P < 0.05) degree of inter-hemisphere FC (interdegree) mainly within ipsilesional somatosensory region and a significantly diminished degree of intra-hemisphere FC (intradegree) (P < 0.05) in ipsilesional primary somatosensory region were observed when stimulating the affected forearm, compared with the unaffected forearm. Conclusions The alteration of cortical connectivity in fine tactile sensation post-stroke was characterized by the compensation from the contralesional hemisphere and distributed attention networks related to involuntary attention. The interhemispheric connectivity could implement the compensation from the contralateral hemisphere to the ipsilesional somatosensory region. Stroke participants also exerted increased cortical activities in fine tactile sensation.