IL-6
Biomarker10 papers3 findings
In human cohorts, IL-6 associates with chronic obstructive pulmonary disease in high-risk individuals and with mortality in elderly COVID-19 patients. Additionally, a review reports that targeting LOX-1 with an antibody decreases IL-6 in a clinical trial.
- Humans2
- Animals3
- Cells2
Interventions
1LOX-1 antibody
downin humans1
1 study
LOX-1 antibody
downin humans1
LOX-1 antibody decreases IL-6 in humans.
Reviewin GOLDILOX-TIMI 69 trial
An Update of Oxidative Stress in Atherosclerosis with Emphasis on the LOX-1-NLRP3 Inflammasome Axis · Current atherosclerosis reports · 29 Sep 2026
Associations
2Chronic obstructive pulmonary disease
upin humans1
1 study
Chronic obstructive pulmonary disease
upin humans1
IL-6 is associated with chronic obstructive pulmonary disease in humans.
Humanshigh-risk individuals (COPD-SQ ≥ 16, preserved lung function)n = 89
Age-linked immune profiles identify distinct risk groups for chronic obstructive pulmonary disease · Journal of inflammation research · 22 Sep 2026
Mortality
upin humans1
1 study
Mortality
upin humans1
IL-6 is associated with mortality in humans.
“Additionally, five cytokines-GRO-α, IL-6, IL-8, IP-10, and TSLP-showed higher levels in non-survivors.”
Humanselderly COVID-19 patientsplasma
Plasma metabolic shifts link to T-cell senescence and mortality in older COVID-19 patients · Biomedicines · 19 Sep 2026
Latest
10Long-term human skin platform models chronic inflammation and senolytic treatments
The culture platform maintained native tissue architecture for four weeks, revealing treatment effects on aged donor tissue that emerged only after prolonged exposure.
Age-linked immune profiles identify distinct risk groups for chronic obstructive pulmonary disease
Clustering four age-associated inflammatory cytokines separated adults into three distinct endotypes tied to early chronic lung disease risk.
Arsenic triggers heart senescence in mice while quercetin counteracts the damage
Exposure to environmental arsenic caused heart dysfunction via the p53 and p21 pathway, which quercetin treatment reversed in cultured rat cardiomyoblasts.
Plasma metabolic shifts link to T-cell senescence and mortality in older COVID-19 patients
Dysregulated phospholipid and bile acid metabolism tracked with cytokine spikes and 180-day mortality, while a specific lipid attenuated senescent markers in cell tests.