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Gut microbe dysbiosis increases repetitive inflammatory responses, leading to an increase in the incidence of colorectal cancer. Recent studies have revealed that specific microbial species directly instigate mutations in the host nucleus DNA, thereby accelerating the progression of colorectal cancer. Given the well-established role of mitochondrial dysfunction in promoting colorectal cancer, it is reasonable to postulate that gut microbes may induce mitochondrial gene mutations, thereby inducing mitochondrial dysfunction. In this review, we focus on gut microbial genotoxins and their known and potential targets in mitochondrial genes. Consequently, we propose that targeted disruption of genotoxin transport pathways may effectively reduce the rate of mitochondrial gene mutations and yield substantial benefits for the prevention of colorectal carcinogenesis.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11406885 | PMC |
http://dx.doi.org/10.1128/msystems.00887-24 | DOI Listing |
Reproduction
October 2025
Maternal and Fetal Health Research Centre, University of Manchester, Manchester, United Kingdom.
In Brief: Advanced maternal age (AMA) is associated with adverse pregnancy outcomes, particularly those associated with placental dysfunction. This study showed that in a mouse model of AMA, male but not female fetuses had increased placental apoptosis and lipid peroxidation, as well as increased mitochondrial content, suggesting that the placentas of male fetuses in AMA mothers adapt to be able to deliver sufficient energy to the fetus.
Abstract: Although advanced maternal age (AMA) increases the risk of fetal growth restriction (FGR) and stillbirth, the mechanisms leading to the placental dysfunction observed in AMA are unknown.
Proc Natl Acad Sci U S A
September 2025
State Key Laboratory of Bioactive Molecules and Druggability Assessment, Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine and New Drugs Research, International Cooperative Laboratory of Traditional Chinese Medicine Modernization and Innovative Drug De
Proliferative retinopathy is a leading cause of irreversible blindness in humans; however, the molecular mechanisms behind the immune cell-mediated retinal angiogenesis remain poorly elucidated. Here, using single-cell RNA sequencing in an oxygen-induced retinopathy (OIR) model, we identified an enrichment of sorting nexin (SNX)-related pathways, with SNX3, a member of the SNX family that is involved in endosomal sorting and trafficking, being significantly upregulated in the myeloid cell subpopulations of OIR retinas. Immunostaining showed that SNX3 expression is markedly increased in the retinal microglia/macrophages of mice with OIR, which is mainly located within and around the neovascular tufts.
View Article and Find Full Text PDFMetabolomics
September 2025
Laboratoire de Biochimie et Biologie Moléculaire, Centre Hospitalier Universitaire, Angers, France.
Introduction: The definition of Leber's hereditary optic neuropathy (LHON) does not take into account a preclinical phase during which the thickness of retinal nerve fiber layer (RNFL) is increased, prior to optic nerve atrophy, reducing the chances of visual recovery.
Objectives: Search for a metabolomic signature characterizing this preclinical phase and identify biomarkers predicting the risk of LHON onset.
Methods And Results: The blood and tear metabolomic profiles of 90 asymptomatic LHON mutation carriers followed for one year will be explored as a function of RNFL thickness and compared to those of a healthy control.
Hum Genet
September 2025
College of Otolaryngology Head and Neck Surgery, Chinese PLA General Hospital, Chinese PLA Medical School, 28 Fuxing Road, Beijing, 100853, China.
Recessive variants in TWNK cause syndromes arising from mitochondrial DNA (mtDNA) depletion. Hearing loss is the most prevalent manifestation in individuals with these disorders. However, the clinical and pathophysiological features have not been fully elucidated.
View Article and Find Full Text PDFMol Biomed
September 2025
National Key Laboratory of Immunity and Inflammation & Institute of Immunology, College of Basic Medical Sciences, Naval Medical University, Shanghai, 200433, China.
Dendritic cells (DCs) play a central role in coordinating immune responses by linking innate and adaptive immunity through their exceptional antigen-presenting capabilities. Recent studies reveal that metabolic reprogramming-especially pathways involving acetyl-coenzyme A (acetyl-CoA)-critically influences DC function in both physiological and pathological contexts. This review consolidates current knowledge on how environmental factors, tumor-derived signals, and intrinsic metabolic pathways collectively regulate DC development, subset differentiation, and functional adaptability.
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