Neutrophils induce paracrine telomere dysfunction and senescence in ROS‐dependent manner is a research paper published in The EMBO Journal (2021). On theSindex it has a DataRank of 0. It has been cited 212 times.
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UKRI | Biotechnology and Biological Sciences Research Council
Grant: BB/K017314/1
Regulation of DNA damage signaling by autophagy in senescence
UKRI | Biotechnology and Biological Sciences Research Council
Grant: BB/L502066/1
The impact of melanocyte senescence on skin ageing
HHS | National Institutes of Health
Grant: P01 AG062413
HHS | National Institutes of Health
Grant: R01 AG050582
Cancer Research UK
Grant: C18342/A23390
UKRI | Medical Research Council
Grant: MR/K0019494/1
UKRI | Medical Research Council
Grant: MR/R023026/1
MICA: Molecular drivers of fibrosis at the hepatic epithelial-mesenchymal barrier
HHS | NIH | National Institute on Aging
Grant: R01 AG 68048
HHS | NIH | National Institute on Aging
Grant: R01 AG068182‐01
HHS | NIH | National Institute on Aging
Grant: R37 AG013925
HHS | NIH | National Center for Advancing Translational Sciences
Grant: UL1 TR0002377
Cancer Research UK
Grant: S_4276
Biotechnology and Biological Sciences Research Council
Grant: BB/S006710/1
NIDDK NIH HHS
Grant: P30 DK084567
NIA NIH HHS
Grant: R01 AG068048
NIA NIH HHS
Grant: R01 AG068182
Cancer Research UK
Grant: 26813
Medical Research Council
Grant: MR/K001949/1
Medical Research Council
Grant: G0900535
Academy of Medical Sciences
Grant: SBF005\1130
NIA NIH HHS
Grant: T32 AG049672
NCATS NIH HHS
Grant: UL1 TR002377
Cancer Research UK
Grant: 23390
National Centre for the Replacement, Refinement and Reduction of Animals in Research
Grant: NC/K000748/1
NCI NIH HHS
Grant: UG3 CA268103
National Institutes of Health
Grant: 3P01AG062413-02S1
Targeting Cellular Senescence to Extend Healthspan
National Institutes of Health
Grant: 5R01AG068048-03
The role of sub-lethal mitochondrial apoptotic stress in cellular senescence
National Institutes of Health
Grant: 3UL1TR002377-04S5
Mayo Clinic Center for Clinical and Translational Science (CCaTS UL1 Supplement - Dr. Regan Theiler)
National Institutes of Health
Grant: 3R37AG013925-16S1
Effect of Aging on Preadipocyte Differentiation
European Commission
Grant: 683000
Cellular and molecular mechanisms of metabolic immune activation triggering non-alcoholic steatohepatitis (NASH) and HCC
National Institutes of Health
Grant: 5P30DK084567-05
CLINICAL CORE
National Institutes of Health
Grant: 5R01AG050582-02
The Role of Somatic Transposition in Age-associated Genomic Instability
National Institutes of Health
Grant: 1R01AG068182-01
Does obesity exacerbate age-related cognitive decline via senescence?
American Association for the Study of Liver Diseases
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
FWCI
17.82
Citation Percentile
1.0%
Citation Trend
Fields of Study
MeSH Terms
Keywords
Sustainable Development Goals
Additional file 1 of Evidence of telomere attrition and a potential role for DNA damage in systemic sclerosis
Additional file 1 of Evidence of telomere attrition and a potential role for DNA damage in systemic sclerosis
Additional file 2 of Evidence of telomere attrition and a potential role for DNA damage in systemic sclerosis
Additional file 2 of Evidence of telomere attrition and a potential role for DNA damage in systemic sclerosis
Additional file 2 of Acetyl-CoA metabolism drives epigenome change and contributes to carcinogenesis risk in fatty liver disease
Additional file 2 of Acetyl-CoA metabolism drives epigenome change and contributes to carcinogenesis risk in fatty liver disease
Additional file 1 of Clinical assessment and molecular mechanism of the upregulation of Toll-like receptor 2 (TLR2) in myocardial infarction
Additional file 1 of Clinical assessment and molecular mechanism of the upregulation of Toll-like receptor 2 (TLR2) in myocardial infarction
Additional file 1 of Acetyl-CoA metabolism drives epigenome change and contributes to carcinogenesis risk in fatty liver disease
Additional file 4 of Acetyl-CoA metabolism drives epigenome change and contributes to carcinogenesis risk in fatty liver disease
Additional file 3 of Acetyl-CoA metabolism drives epigenome change and contributes to carcinogenesis risk in fatty liver disease
Additional file 4 of Acetyl-CoA metabolism drives epigenome change and contributes to carcinogenesis risk in fatty liver disease
Additional file 1 of Acetyl-CoA metabolism drives epigenome change and contributes to carcinogenesis risk in fatty liver disease
Additional file 3 of Acetyl-CoA metabolism drives epigenome change and contributes to carcinogenesis risk in fatty liver disease