Oncogene. 2025 Apr 1. doi: 10.1038/s41388-025-03363-7. Online ahead of print.

NO ABSTRACT

PMID:40169919 | DOI:10.1038/s41388-025-03363-7

Nat Med. 2025 Apr 1. doi: 10.1038/s41591-025-03532-x. Online ahead of print.

ABSTRACT

Disease progression is a substantial challenge in patients with non-Hodgkin lymphoma (NHL) undergoing chimeric antigen receptor T cell (CAR-T) therapy. Here we present InflaMix (INFLAmmation MIXture Model), an unsupervised quantitative model integrating 14 pre-CAR-T infusion laboratory and cytokine measures capturing inflammation and end-organ function. Developed using a cohort of 149 patients with NHL, InflaMix revealed an inflammatory signature associated with a high risk of CAR-T treatment failure, including increased hazard of death or relapse (hazard ratio, 2.98; 95% confidence interval, 1.60-4.91; P < 0.001). Three independent cohorts comprising 688 patients with NHL from diverse treatment centers were used to validate our approach. InflaMix consistently and reproducibly identified patients with a higher likelihood of disease relapse and mortality, and it provided supplementary predictive value beyond established prognostic markers, including tumor burden. Moreover, InflaMix exhibited robust performance in cases with missing data, maintaining accuracy when considering only six readily available laboratory measures. These findings show that InflaMix is a valuable tool for point-of-care clinical decision-making in patients with NHL undergoing CAR-T therapy.

PMID:40169864 | DOI:10.1038/s41591-025-03532-x

Mol Psychiatry. 2025 Apr 2. doi: 10.1038/s41380-025-02977-3. Online ahead of print.

ABSTRACT

Altered levels of human plasma metabolites have been implicated in the etiology of bipolar disorder (BD). However, the causality between metabolites and the disease was not well described. We performed a bidirectional metabolome-wide Mendelian randomization (MR) analysis to evaluate the potential causal relationships between 871 plasma metabolites and BD. We used DrugBank and ChEMBL to evaluate whether related metabolites are potential therapeutic targets. Finally, Bayesian colocalization analysis was performed to identify shared genomic loci BD and identified metabolites. Our MR results showed that six metabolites were significantly associated with a reduced risk of BD, including arachidonate (20:4n6) (OR: 0.90, 95% CI: 0.84-0.95) and sphingomyelin (d18:2/24:1, d18:1/24:2) (OR: 0.92, 95% CI: 0.87-0.96), while five metabolites were significantly associated with an increased risk of BD, including 1-palmitoyl-2-linoleoyl-GPE (16:0/18:2) (OR: 1.09, 95% CI: 1.05-1.13). However, our reverse MR analysis showed that BD was not associated with the levels of any metabolite. Additionally, the leave-one-out analysis revealed SNPs within chromosome 11 loci harboring MYRF, FADS1, and FADS2 as ones with the potential to influence partial causal effects. Druggability evaluation showed that 10 of the BD-related metabolites, such as sphingomyelin and cytidine, have been targeted by pharmacologic intervention. Colocalization analysis highlighted one colocalized region (chromosome 11q12) shared by 11 metabolites and BD and pointed to some genes as possible players, including FADS1, FADS2, FADS3, and SYT7. Our study supported a causal role of plasma metabolites in the susceptibility to BD, and the identified metabolites may provide a new avenue for the prevention and treatment of BD.

PMID:40169804 | DOI:10.1038/s41380-025-02977-3

Br J Cancer. 2025 Apr 1. doi: 10.1038/s41416-025-02987-6. Online ahead of print.

ABSTRACT

BACKGROUND: Individualized treatment decisions for multiple myeloma (MM) patients require accurate risk stratification that accounts for patient-specific consequences of cytogenetic abnormalities on disease progression.

METHODS: Previously, SYstems Genetic Network AnaLysis (SYGNAL) of multi-omics tumor profiles from 881 MM patients generated a mmSYGNAL network of transcriptional programs underlying disease progression across MM subtypes. Here, through machine learning on activity profiles of mmSYGNAL programs we have generated a unified framework of cytogenetic subtype-specific models for individualized risk classifications and prediction of treatment response.

RESULTS: Testing on 1,367 patients across five independent cohorts demonstrated that the framework of mmSYGNAL risk models significantly outperformed cytogenetics, International Staging System, and multi-gene biomarker panels in predicting PFS at primary diagnosis, pre- and post-transplant and even after multiple relapses, making it useful for individualized risk assessment throughout the disease trajectory. Further, treatment response predictions were significantly concordant with efficacy of 67 drugs in killing myeloma cells from eight relapsed refractory patients. The model also provided new insights into matching MM patients to drugs used in standard of care, at relapse, and in clinical trials.

CONCLUSION: Activities of transcriptional programs offer significantly better prognostic and predictive assessments of treatments across different stages of MM in an individual patient.

PMID:40169765 | DOI:10.1038/s41416-025-02987-6

Sci Rep. 2025 Apr 1;15(1):11090. doi: 10.1038/s41598-025-86745-x.

ABSTRACT

The Mayombe and Batéké Plateau ecozones of the Democratic Republic of Congo (DRC) are experiencing differentiated deforestation and forest degradation, together with a trend toward homogenization of their agricultural diversity. These may undermine efforts to sustainably reverse household food, nutrition, and livelihood insecurity. In this context, this study seeks to assess the importance of yam in the role of agrobiodiversity among populations in the two contrasting ecozones. A sample of 351 households was surveyed. A dataset of about 202 testimonies from six focus groups and observations in 86 peasant agroforestry fields was also analyzed using descriptive statistics, correlation and regression, and calculations of different indices of crop importance. Overall, plant, animal, and fish species represent respectively 60.9%, 26.7% and 12.4% of genetic resources. About 50 of 72 species of these resources are found in both study areas. Regarding the overall use of species, the five top-ranked species that were utilized as food included Manihot esculenta, followed by Arachis hypogaea, Zea mays, Dioscorea alata, and Musa acuminata. Living in the Mayombe ecozone increases the household's preference for growing yams by up to 5.7 times. Population density was correlated with agricultural diversity. Villages with a high population density showed greater crop diversity than those with a low population density. In short, yam remains an important but under-represented crop, the contribution of which could be increased to secure sustainable livelihoods through biodiversity-rich peasant agroforestry systems.

PMID:40169681 | DOI:10.1038/s41598-025-86745-x

Nat Commun. 2025 Apr 1;16(1):3110. doi: 10.1038/s41467-025-58462-6.

ABSTRACT

Ribonucleases (RNases) are ubiquitous enzymes that process or degrade RNA, essential for cellular functions and immune responses. The EndoU-like superfamily includes endoribonucleases conserved across bacteria, eukaryotes, and certain viruses, with an ancient evolutionary link to the ribonuclease A-like superfamily. Both bacterial EndoU and animal RNase A share a similar fold and function independently of cofactors. In contrast, the eukaryotic EndoU catalytic domain requires divalent metal ions for catalysis, possibly due to an N-terminal extension near the catalytic core. In this study, we use biophysical and computational techniques along with in vitro assays to investigate the calcium-dependent activation of human EndoU. We determine the crystal structure of EndoU bound to calcium and find that calcium binding remote from the catalytic triad triggers water-mediated intramolecular signaling and structural changes, activating the enzyme through allostery. Calcium binding involves residues from both the catalytic core and the N-terminal extension, indicating that the N-terminal extension interacts with the catalytic core to modulate activity in response to calcium. Our findings suggest that similar mechanisms may be present across all eukaryotic EndoUs, highlighting a unique evolutionary adaptation that connects endoribonuclease activity to cellular signaling in eukaryotes.

PMID:40169637 | DOI:10.1038/s41467-025-58462-6

Nat Commun. 2025 Apr 1;16(1):3134. doi: 10.1038/s41467-025-57549-4.

ABSTRACT

The direct reduction of CO2 into one-carbon molecules is key to highly efficient biological CO2-fixation. However, this strategy is currently restricted to anaerobic organisms and low redox potentials. In this study, we introduce the CORE cycle, a synthetic metabolic pathway that converts CO2 to formate at aerobic conditions and ambient CO2 levels, using only NADPH as a reductant. Combining theoretical pathway design and analysis, enzyme bioprospecting and high-throughput screening, modular assembly and adaptive laboratory evolution, we realize the CORE cycle in vivo and demonstrate that the cycle supports growth of E. coli by supplementing C1-metabolism and serine biosynthesis from CO2. We further analyze the theoretical potential of the CORE cycle as a new entry-point for carbon in photorespiration and autotrophy. Overall, our work expands the solution space for biological carbon reduction, offering a promising approach to enhance CO2 fixation processes such as photosynthesis, and opening avenues for synthetic autotrophy.

PMID:40169551 | DOI:10.1038/s41467-025-57549-4

G3 (Bethesda). 2025 Apr 2:jkaf062. doi: 10.1093/g3journal/jkaf062. Online ahead of print.

ABSTRACT

Telomeres are eukaryotic chromosome end structures that guard against sequence loss and aberrant chromosome fusions. Telomeric repeat motifs (TRMs), the minimal repeating unit of a telomere, vary from species to species, with some evolutionary clades experiencing a rapid sequence divergence. To explore the full scope of this evolutionary divergence, many bioinformatic tools have been developed to infer novel TRMs using repetitive sequence search on short sequencing reads. However, novel telomeric motifs remain unidentified in up to half of the sequencing libraries assayed with these tools. A possible reason may be that short reads, derived from extensively sheared DNA, preserve little to no positional context of the repetitive sequences assayed. On the other hand, if a sequencing read is sufficiently long, telomeric sequences must appear at either end rather than in the middle. The TeloSearchLR algorithm relies on this to help identify novel TRMs on long reads, in many cases where short-read search tools have failed. In addition, we demonstrate that TeloSearchLR can reveal unusually long telomeric motifs not maintained by telomerase, and it can also be used to anchor terminal scaffolds in new genome assemblies.

PMID:40169380 | DOI:10.1093/g3journal/jkaf062

Cell Host Microbe. 2025 Mar 25:S1931-3128(25)00088-5. doi: 10.1016/j.chom.2025.03.005. Online ahead of print.

ABSTRACT

Many eukaryotic viruses require membrane-bound compartments for replication, but no such organelles are known to be formed by prokaryotic viruses. Bacteriophages of the Chimalliviridae family sequester their genomes within a phage-generated organelle, the phage nucleus, which is enclosed by a lattice of the viral protein ChmA. We show that inhibiting phage nucleus formation arrests infections at an early stage in which the injected phage genome is enclosed within a membrane-bound early phage infection (EPI) vesicle. Early phage genes are expressed from the EPI vesicle, demonstrating its functionality as a prokaryotic, transcriptionally active, membrane-bound organelle. We also show that the phage nucleus is essential, with genome replication beginning after the injected DNA is transferred from the EPI vesicle to the phage nucleus. Our results show that Chimalliviridae require two sophisticated subcellular compartments of distinct compositions and functions that facilitate successive stages of the viral life cycle.

PMID:40168997 | DOI:10.1016/j.chom.2025.03.005

Cell Host Microbe. 2025 Mar 25:S1931-3128(25)00091-5. doi: 10.1016/j.chom.2025.03.008. Online ahead of print.

ABSTRACT

Plasmodium parasites undergo development and replication within hepatocytes before infecting erythrocytes and initiating clinical malaria. Although type I interferons (IFNs) are known to hinder Plasmodium infection within the liver, the underlying mechanisms remain unclear. Here, we describe two IFN-I-driven hepatocyte antimicrobial programs controlling liver-stage malaria. First, oxidative defense by NADPH oxidases 2 and 4 triggers a pathway of lysosomal fusion with the parasitophorous vacuole (PV) to help clear Plasmodium. Second, guanylate-binding protein (GBP) 1-mediated disruption of the PV activates the caspase-1 inflammasome, inducing pyroptosis to remove infected host cells. Remarkably, both human and mouse hepatocytes enlist these cell-autonomous immune programs to eliminate Plasmodium, with their pharmacologic or genetic inhibition leading to profound malarial susceptibility in vivo. In addition to identifying IFN-I-mediated cell-autonomous immune circuits controlling Plasmodium infection in the hepatocytes, our study also extends the understanding of how non-immune cells are integral to protective immunity against malaria.

PMID:40168996 | DOI:10.1016/j.chom.2025.03.008

Eur J Cancer. 2025 Mar 30;220:115393. doi: 10.1016/j.ejca.2025.115393. Online ahead of print.

ABSTRACT

The annual Immuno-Oncology "Think Tank" held in October 2023 in Siena reviewed the rapidly evolving systems-biological approaches which are now providing a deeper understanding of tumor and tumor microenvironment heterogeneity. Based on this understanding opportunities for novel therapies may be identified to overcome resistance to immunotherapy. There is increasing evidence that malignant disease processes are not limited to purely intracellular or genetic events but constitute a dynamic interaction between the host and disease. Tumor responses are influenced by many host tissue determinants across different cellular compartments, which can now be investigated by high-throughput molecular profiling technologies, often labelled with a suffix "-omics". "Omics" together with ever increasing computational power, fast developments in machine learning, and high-resolution detection tools offer an unrivalled opportunity to connect high-dimensional data and create a holistic view of disease processes in cancer. This review describes advances in several state-of-the-art "-omics" approaches with perspectives on how these can be applied to the clinical development of new immunotherapeutic strategies and ultimately adopted in clinical practice.

PMID:40168935 | DOI:10.1016/j.ejca.2025.115393

PLoS Biol. 2025 Apr 1;23(4):e3003062. doi: 10.1371/journal.pbio.3003062. eCollection 2025 Apr.

ABSTRACT

The human fungal pathogen Candida tropicalis is widely distributed in clinical and natural environments. It is known to be an obligate diploid organism with an incomplete and atypical sexual cycle. Azole-resistant C. tropicalis isolates have been observed with increasing prevalence in many countries in recent years. Here, we report that tebuconazole (TBZ), a triazole fungicide widely used in agriculture, can induce ploidy plasticity and the formation of haploid cells in C. tropicalis. The evolved C. tropicalis strains with ploidy variations exhibit a cross-resistance between TBZ and standard azoles used in clinical settings (such as fluconazole and voriconazole). Similar to its diploid cells, these newly discovered C. tropicalis haploid cells are capable of undergoing filamentation, white-opaque switching, and mating. However, compared to its diploid cells, these haploid C. tropicalis cells grow more slowly under in vitro culture conditions and are less virulent in a mouse model of systemic infection. Interestingly, flow cytometry analysis of a clinical strain with extremely low genome heterozygosity indicates the existence of natural C. tropicalis haploids. Discovery of this C. tropicalis haploid state sheds new light into the biology and genetic plasticity of C. tropicalis and could provide the framework for the development of new genetic tools in the field.

PMID:40168394 | DOI:10.1371/journal.pbio.3003062

Proc Natl Acad Sci U S A. 2025 Apr 8;122(14):e2412818122. doi: 10.1073/pnas.2412818122. Epub 2025 Apr 1.

ABSTRACT

The tumor microenvironment (TME) encompasses various cell types, blood and lymphatic vessels, and noncellular constituents like extracellular matrix (ECM) and cytokines. These intricate interactions between cellular and noncellular components contribute to the development of a malignant TME, such as immunosuppressive, desmoplastic, angiogenic conditions, and the formation of a niche for cancer stem cells, but there is limited understanding of the specific subtypes of stromal cells involved in this process. Here, we utilized p16-CreERT2-tdTomato mouse models to investigate the signaling networks established by senescent cancer stromal cells, contributing to the development of a malignant TME. In pancreatic ductal adenocarcinoma (PDAC) allograft models, these senescent cells were found to promote cancer fibrosis, enhance angiogenesis, and suppress cancer immune surveillance. Notably, the selective elimination of senescent cancer stromal cells improves the malignant TME, subsequently reducing tumor progression in PDAC. This highlights the antitumor efficacy of senolytic treatment alone and its synergistic effect when combined with conventional chemotherapy. Taken together, our findings suggest that the signaling crosstalk among senescent cancer stromal cells plays a key role in the progression of PDAC and may be a promising therapeutic target.

PMID:40168129 | DOI:10.1073/pnas.2412818122

Mol Ecol Resour. 2025 Apr 1:e14110. doi: 10.1111/1755-0998.14110. Online ahead of print.

ABSTRACT

The percomorph fish clade Gobioidei is a suborder that comprises over 2200 species distributed in nearly all aquatic habitats. To understand the genetics underlying their species diversification, we sequenced and annotated the genome of the loach goby, Rhyacichthys aspro, an early-diverging group, and compared it with nine additional Gobioidei species. Within Gobioidei, the loach goby possesses the smallest genome at 594 Mb, and a rise in species diversity from early-diverging to more recently diverged lineages is mirrored by enlarged genomes and a higher presence of transposable elements (TEs), particularly DNA transposons. These DNA transposons are enriched in genic and regulatory regions and their copy number increase is strongly correlated with substitution rate, suggesting that DNA repair after transposon excision/insertion leads to nearby mutations. Consequently, the proliferation of DNA transposons might be the crucial driver of Gobioidei diversification and adaptability. The loach goby genome also points to mechanisms of ecological adaptation. It contains relatively few genes for lateral line development but an overrepresentation of synaptic function genes, with genes putatively under selection linked to synapse organisation and calcium signalling, implicating a sensory system distinct from other Gobioidei species. We also see an overabundance of genes involved in neurocranium development and renal function, adaptations likely connected to its flat morphology suited for strong currents and an amphidromous life cycle. Comparative analyses with hill-stream loaches and the European eel reveal convergent adaptations in body shape and saltwater balance. These findings shed new light on the loach goby's survival mechanisms and the broader evolutionary trends within Gobioidei.

PMID:40168108 | DOI:10.1111/1755-0998.14110

Methods Mol Biol. 2025;2914:275-302. doi: 10.1007/978-1-0716-4462-1_20.

ABSTRACT

Cerebrospinal fluid (CSF) is a source of valuable information concerning brain disorders. The technical advances of high throughput omics platforms to analyze body fluids can generate a huge amount of data, whose translation of the biological meaning can be a challenge. Several bioinformatics tools have emerged to help handle this data from a systems biology perspective. Herein, we describe a step-by-step tutorial for CSF proteome data analysis in the set of neurodegenerative diseases using: (i) ShinyGO webtool to perform functional enrichment analysis envisioning the characterization of the biological pathways and processes deregulated in neurodegenerative diseases including Alzheimer's and Parkinson's diseases; (ii) Cytoscape to map disease-specific proteins based on evidence from proteomics; (iii) DisGeNET to identify the proteins more strongly and more specifically associated with neurodegenerative diseases to date; (iv) STRING to identify putative therapeutic targets through a combined protein-protein interaction and network topological analyses. This step-by-step guide might help researchers to better characterize disease pathogenesis and to identify putative disease biomarkers and therapeutic targets.

PMID:40167925 | DOI:10.1007/978-1-0716-4462-1_20

Metabolomics. 2025 Apr 1;21(2):48. doi: 10.1007/s11306-025-02247-x.

NO ABSTRACT

PMID:40167843 | DOI:10.1007/s11306-025-02247-x

Semin Immunopathol. 2025 Apr 1;47(1):23. doi: 10.1007/s00281-025-01049-6.

ABSTRACT

Barrier organs such as the gastrointestinal tract, lungs, and skin are colonized by diverse microbial strains, including bacteria, viruses, and fungi. These microorganisms, collectively known as the commensal microbiota, play critical roles in maintaining health by defending against pathogens, metabolizing nutrients, and providing essential metabolites. In the gut, commensal-derived antigens are frequently sensed by the intestinal immune system. Maintaining tolerance toward these beneficial microbial species is crucial, as failure to do so can lead to chronic inflammatory conditions like inflammatory bowel disease (IBD) and can even affect systemic immune or metabolic health. The immune system carefully regulates responses to commensals through various mechanisms, including the induction of anti-inflammatory CD4⁺ T cell responses. Foxp3⁺ regulatory T cells (Foxp3+ Tregs) and Type 1 regulatory T cells (Tr1) play a major role in promoting tolerance, as both cell types can produce the anti-inflammatory cytokine IL-10. In addition to these regulatory T cells, effector T cell subsets, such as Th17 cells, also adopt anti-inflammatory functions within the intestine in response to the microbiota. This process of anti-inflammatory CD4+ T cell induction is heavily influenced by the microbiota and their metabolites. Microbial metabolites affect intestinal epithelial cells, promoting the secretion of anti-inflammatory mediators that create a tolerogenic environment. They also modulate intestinal dendritic cells (DCs) and macrophages, inducing a tolerogenic state, and can interact directly with T cells to drive anti-inflammatory CD4⁺ T cell functionality. The disrupted balance of these signals may result in chronic inflammation, with broader implications for systemic health. In this review, we highlight the intricate interplays between commensal microorganisms and the immune system in the gut. We discuss how the microbiota influences the differentiation of commensal-specific anti-inflammatory CD4⁺ T cells, such as Foxp3⁺ Tregs, Tr1 cells, and Th17 cells, and explore the mechanisms through which microbial metabolites modulate these processes. We further discuss the innate signals that prime and commit these cells to an anti-inflammatory fate.

PMID:40167791 | DOI:10.1007/s00281-025-01049-6

Funct Integr Genomics. 2025 Apr 1;25(1):78. doi: 10.1007/s10142-025-01588-z.

ABSTRACT

Metabolic engineering of lipids in crops presents a promising strategy to enhance resilience against environmental stressors while improving nutritional quality. By manipulating key enzymes in lipid metabolism, introducing novel genes, and utilizing genome editing technologies, researchers have improved crop tolerance to abiotic stresses such as drought, salinity, and extreme temperatures. Additionally, modified lipid pathways contribute to resistance against biotic stresses, including pathogen attacks and pest infestations. Engineering multiple stress-resistance traits through lipid metabolism offers a holistic approach to strengthening crop resilience amid changing environmental conditions. Beyond stress tolerance, lipid engineering enhances the nutritional profile of crops by increasing beneficial lipids such as omega-3 fatty acids, vitamins, and antioxidants. This dual approach not only improves crop yield and quality but also supports global food security by ensuring sustainable agricultural production. Integrating advanced biotechnological tools with a deeper understanding of lipid biology paves the way for developing resilient, nutrient-rich crops capable of withstanding climate change and feeding a growing population.

PMID:40167787 | DOI:10.1007/s10142-025-01588-z

Adv Sci (Weinh). 2025 Apr 1:e2412921. doi: 10.1002/advs.202412921. Online ahead of print.

ABSTRACT

HDAC6 is integral to the regulation of primary cilia, which are specialized structures that serve as crucial signaling hubs for cellular communication and environmental response. These ciliary functions are essential for maintaining cellular homeostasis and orchestrating developmental processes. Dysregulation of HDAC6 activity is implicated in ciliopathies, a group of disorders characterized by defective ciliary structure or function, resulting in widespread organ involvement and significant morbidity. This review provides a comprehensive examination of the molecular dynamics of HDAC6 in the context of ciliogenesis and ciliopathies, emphasizing its dual role in the deacetylation of microtubules and regulation of the ciliary axoneme. Furthermore, HDAC6 interacts with key signaling molecules, modulating processes ranging from cell cycle regulation to inflammatory responses, which highlights its central role in cellular physiology and pathology. The therapeutic potential of HDAC6 inhibitors has been explored, with promising results in various disease models, including retinal and renal ciliopathies, highlighting their ability to restore normal ciliary function. This analysis not only underscores the critical importance of HDAC6 in maintaining ciliary integrity but also illustrates how targeting the HDAC6-cilia axis could provide a groundbreaking approach to treating these complex disorders. In doing so, this review sets the stage for future investigations into HDAC6-targeted therapies, potentially transforming the clinical management of ciliopathies and significantly improving patient outcomes.

PMID:40167251 | DOI:10.1002/advs.202412921

J Gerontol A Biol Sci Med Sci. 2025 Mar 28:glaf053. doi: 10.1093/gerona/glaf053. Online ahead of print.

ABSTRACT

Ageing-associated cognitive decline affects more than half of those in long-term residential aged care. Emerging evidence suggests that gut microbiome-host interactions influence the effects of modifiable risk factors. We investigated the relationship between gut microbiome characteristics and severity of cognitive impairment CI in 159 residents of long-term aged care. Severe CI was associated with a significantly increased abundance of proinflammatory bacterial species, including Methanobrevibacter smithii and Alistipes finegoldii, and decreased relative abundance of beneficial bacterial clades. Severe CI was associated with increased microbial capacity for methanogenesis, and reduced capacity for synthesis of short-chain fatty acids, neurotransmitters glutamate and gamma-aminobutyric acid, and amino acids required for neuro-protective lysosomal activity. These relationships were independent of age, sex, antibiotic exposure, and diet. Our findings implicate multiple gut microbiome-brain pathways in ageing-associated cognitive decline, including inflammation, neurotransmission, and autophagy, and highlight the potential to predict and prevent cognitive decline through microbiome-targeted strategies.

PMID:40166866 | DOI:10.1093/gerona/glaf053