To lessen the "wear and tear" of existence, cells have evolved mechanisms that continuously sense DNA lesions, repair DNA damage and restore the compromised genome back to its native form. Besides genome maintenance pathways, multicellular organisms may also employ adaptive and innate immune mechanisms to guard themselves against bacteria or viruses. Recent evidence points to reciprocal interactions between DNA repair, DNA damage responses and aspects of immunity; both self-maintenance and defense responses share a battery of common players and signaling pathways aimed at safeguarding our bodily functions over time. In the short-term, this functional interplay would allow injured cells to restore damaged DNA templates or communicate their compromised state to the microenvironment. In the long-term, however, it may result in the (premature) onset of age-related degeneration, including cancer. Here, we discuss the beneficial and unrewarding outcomes of DNA damage-driven inflammation in the context of tissue-specific pathology and disease progression.
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http://dx.doi.org/10.3389/fgene.2016.00187 | DOI Listing |
BMC Nephrol
January 2025
Faculty of Medicine and Biomedical Sciences, University of Yaoundé 1, Yaoundé, Cameroon.
Background And Hypothesis: Gut dysbiosis characterized by an imbalance in pathobionts (Enterobacter, Escherichia and Salmonella) and symbionts (Bifidobacterium, Lactobacillus and Prevotella) can occur during chronic kidney disease (CKD) progression. We evaluated the associations between representative symbionts (Bifidobacterium and Lactobacillus) and pathobionts (Enterobacteriaceae) with kidney function in persons with autosomal dominant polycystic kidney disease (ADPKD).
Methods: In this cross-sectional study, 29 ADPKD patients were matched to 15 controls at a 2:1 ratio.
J Fluoresc
January 2025
Department of Chemistry, Faculty of Science, Chulalongkorn University, Bangkok, Phayathai Road Pathumwan, 10330, Thailand.
This study presents a new highly sensitive and specific time-resolved fluoroimmunoassay (TRFIA) for the measurement of trace amounts of the urinary 8-hydroxy-2`-deoxyguanosine (8-OHdG) which is a biomarker for oxidative stress on DNA. The assay relied on a competitive binding approach and a mouse monoclonal antibody which recognized 8-OHdG with high specificity. In this assay, 8-OHdG conjugated with bovine serum albumin protein (8-OHdG-BSA) was employed as a solid phase antigen.
View Article and Find Full Text PDFInflamm Res
January 2025
Department of Anesthesiology, Critical Care, and Surgery, Duke University School of Medicine, Durham, NC, USA.
Background: Mitochondria generate the adenosine triphosphate (ATP) necessary for eukaryotic cells, serving as their primary energy suppliers, and contribute to host defense by producing reactive oxygen species. In many critical illnesses, including sepsis, major trauma, and heatstroke, the vicious cycle between activated coagulation and inflammation results in tissue hypoxia-induced mitochondrial dysfunction, and impaired mitochondrial function contributes to thromboinflammation and cell death.
Methods: A computer-based online search was performed using the PubMed and Web of Science databases for published articles concerning sepsis, trauma, critical illnesses, cell death, mitochondria, inflammation, coagulopathy, and organ dysfunction.
Inflamm Res
January 2025
Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, 250014, Shandong, People's Republic of China.
Cardiovascular diseases (CVDs) continue to be a substantial global healthcare burden despite considerable progress in therapies. The inflammatory response during the progression of CVD has attracted considerable attention. Mitochondria serve as the principal energy source for the heart.
View Article and Find Full Text PDFNat Cell Biol
January 2025
Genome Integrity Unit, Children's Medical Research Institute, University of Sydney, Westmead, New South Wales, Australia.
Double-strand breaks (DSBs) can initiate mitotic catastrophe, a complex oncosuppressive phenomenon characterized by cell death during or after cell division. Here we unveil how cell cycle-regulated DSB repair guides disparate cell death outcomes through single-cell analysis of extended live imaging. Following DSB induction in S or G2, passage of unresolved homologous recombination intermediates into mitosis promotes non-immunogenic intrinsic apoptosis in the immediate attempt at cell division.
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