Toll-Like Receptors in Stem/Progenitor Cells

Sallustio, Fabio; Picerno, Angela; Tatullo, Marco; Rampino, Antonio; Rengo, Carlo; Valletta, Alessandra; Torretta, Silvia; Falcone, Rosa

doi:10.1007/164_2021_539

Cited by 4 publications

(2 citation statements)

References 164 publications

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“…The authors declared no conflict of interests. and T lymphocytes was severely affected [18][19][20] , just in agreement with the results mentioned in this study. It was suggested because excessive LPS exposure induce aberrant expansion of HSCs but permanently impeded the normal self-renew and differentiation capacity [20,21] .…”

Section: Author Contributionssupporting

confidence: 93%

Identification of Key Molecular Signaling Pathways and Therapeutic Targets in Sepsis Shock

Wang,

Zhao,

Zhang

et al. 2023

IJPS

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Sepsis shock was associated with worse mortality than common sepsis caused by disseminated infection. The present study had shown that repression of adaptive immunity was a characteristic of sepsis shock rather than sepsis, but the mechanism in which it exerted the adverse reaction was still need to be studied. In this study, we first employed weighted gene co-expression network analysis for acquiring the key modules with sepsis shock. Then, the differentially expressed genes and transcription factors were screened in the module for further function analysis, protein-protein interaction network building and long noncoding ribonucleic acid-micro ribonucleic acid-transcription factor network study. The study strengthened the concept that adaptive immune repression typically featured the sepsis shock concerning antigen presentation via major histocompatibility complex class II, T-cell activation and T-cell depletion. Among which T-cell depletion ranked as an overwhelming contributor to sepsis shock outcome. The transcription factor tumor protein P53, forkhead box protein O1 and GATA binding protein 3 served as the master regulator for the T-cell depletion process mainly through driving hematopoietic stem cells out of quiescence to unrestrained hematopoietic stem cell expansion with detrimental deoxyribonucleic acid damage, which greatly decreased hematopoietic stem cells long-term differentiation potential into T lymphocyte hierarchy. The study enlightened that manipulating the expression level of tumor protein P53, forkhead box protein O1 and GATA binding protein 3 to an optimized state will guarantee the T cell replenishment for fighting sepsis shock, which might support a potential efficient therapeutic way for sepsis shock treatment.

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Section: Author Contributionssupporting

confidence: 93%

Identification of Key Molecular Signaling Pathways and Therapeutic Targets in Sepsis Shock

Wang,

Zhao,

Zhang

et al. 2023

IJPS

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“…The engagement of different TLR ligands leads to unique cytokine production ( 159 ). It is likely that cross-talk within various TLR pathways is highly complex and contains many unknowns ( 160 ). Although there are many challenges in developing drugs and balancing TLR signaling, in consideration of molecular targeting therapy against TLRs and signaling molecules might be a promising approach in clinical treatment, many research centers and pharmaceutical companies are expending extensive efforts to develop TLRs modulators.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Toll-like receptors in cardiac hypertrophy

Zhang

Dong

et al. 2023

Front. Cardiovasc. Med.

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Toll-like receptors (TLRs) are a family of pattern recognition receptors (PRRs) that can identify pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). TLRs play an important role in the innate immune response, leading to acute and chronic inflammation. Cardiac hypertrophy, an important cardiac remodeling phenotype during cardiovascular disease, contributes to the development of heart failure. In previous decades, many studies have reported that TLR-mediated inflammation was involved in the induction of myocardium hypertrophic remodeling, suggesting that targeting TLR signaling might be an effective strategy against pathological cardiac hypertrophy. Thus, it is necessary to study the mechanisms underlying TLR functions in cardiac hypertrophy. In this review, we summarized key findings of TLR signaling in cardiac hypertrophy.

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