ArticleShock (Augusta, Ga.)2010
Deficiency of Bid protein reduces sepsis-induced apoptosis and inflammation, while improving septic survival.
Article in Shock (Augusta, Ga.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Regulated cell death in sepsis-associated liver injury: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Mitochondrial dysfunction in sepsis: mechanisms and therapeutic perspectives.Critical care (London, England) · 2024Review
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Article
- Parenteral succinate reduces levels of reactive oxygen species without changing serum caspase-3 levels in septic rats.Anaesthesiology intensive therapy · 2022Article
- Malvidin alleviates mitochondrial dysfunction and ROS accumulation through activating AMPK-α/UCP2 axis, thereby resisting inflammation and apoptosis in SAE mice.Frontiers in pharmacology · 2022Article
- Survival and Pulmonary Injury After Neonatal Sepsis: PD1/PDL1's Contributions to Mouse and Human Immunopathology.Frontiers in immunology · 2021Article
- Serum reactive oxygen species and apoptosis markers in septic patients.Anaesthesiology intensive therapy · 2021Article
- Molecular Pathway of Psoralidin-Induced Apoptosis in HepG2 Cell Line.Chinese journal of integrative medicine · 2019Article
- Metabolic Inflammatory Complex in Sepsis: Septic Cachexia as a Novel Potential Therapeutic Target.Shock (Augusta, Ga.) · 2017Review
- A Novel Role for Programmed Cell Death Receptor Ligand-1 (PD-L1) in Sepsis-Induced Intestinal Dysfunction.Molecular medicine (Cambridge, Mass.) · 2017Article
- Contribution of programmed cell death receptor (PD)-1 to Kupffer cell dysfunction in murine polymicrobial sepsis.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- BID Mediates Oxygen-Glucose Deprivation-Induced Neuronal Injury in Organotypic Hippocampal Slice Cultures and Modulates Tissue Inflammation in a Transient Focal Cerebral Ischemia Model without Changing Lesion Volume.Frontiers in cellular neuroscience · 2016Article
- CD28 homodimer interface mimetic peptide acts as a preventive and therapeutic agent in models of severe bacterial sepsis and gram-negative bacterial peritonitis.The Journal of infectious diseases · 2015Article
- Revisiting caspases in sepsis.Cell death & disease · 2014Review
- The new normal: immunomodulatory agents against sepsis immune suppression.Trends in molecular medicine · 2014Review
- Article
- A prospective analysis of lymphocyte phenotype and function over the course of acute sepsis.Critical care (London, England) · 2012Article
- Splenocyte apoptosis and autophagy is mediated by interferon regulatory factor 1 during murine endotoxemia.Shock (Augusta, Ga.) · 2012Article
- Platelets induce apoptosis during sepsis in a contact-dependent manner that is inhibited by GPIIb/IIIa blockade.PloS one · 2012Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Increased apoptotic cell death is believed to play a pathological role in patients with sepsis and experimental animals. Apoptosis can be induced by either a cell death receptor (extrinsic) or a mitochondrial (intrinsic) pathway. Bid, a proapoptotic member of the Bcl-2 family, is thought to mediate the cross talk between the extrinsic and intrinsic pathways of apoptosis; however, little is known about the action of Bid in the development of apoptosis and organ-specific tissue damage/cell death as seen in polymicrobial sepsis. Our results show that after the onset of sepsis, tBid (the active form of Bid) is significantly increased in mitochondrial fractions of the thymus, spleen, Peyer patches, and liver, and that Fas or FasL deficiency blocks Bid activation in various tissues after septic challenge. Increased Bid activation is correlated with increased active caspase-3, caspase-9, and apoptosis during sepsis. Bid-deficient mice exhibit significantly reduced apoptosis in the thymus, spleen, and Peyer patches compared with background mice after sepsis. Furthermore, Bid-deficient mice had significantly reduced systemic and local inflammatory cytokine levels and improved survival after sepsis. These data support not only the contribution of Bid to sepsis-induced apoptosis and the onset of septic morbidity/mortality, but also the existence of a bridge between extrinsic apoptotic signals, e.g., FasL:Fas, TNF:TNFR, and so on, and the intrinsic mitochondrial pathway via Bid-tBid activation during sepsis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.