From:  Janus-faced role of anti-infective drugs: a revisit through the lens of vascular ageing

 Risk-of-bias assessment of mixed studies combining in vitro, animal, and/or translational models to evaluate anti-infective drugs and vascular ageing.

Ref #Study typeDrug/ClassModel/PopulationTools usedKey bias domains (summary)Overall riskAgeing effects (biomarkers)
[42]MixedAntibiotic (salinomycin)Senescent cancer cells (mouse + in vitro)SYRCLE + narrativeRandomization not detailed; selective reporting; high-dose in vitro armSome concernsInduced immune destruction of senescent cancer cells; ↓ SA-β-gal; ↑ immune clearance
[52]MixedBactericidal antibioticsMammalian cells + animal validationNarrative + SYRCLENo blinding in animal arm; supratherapeutic dosing in vitroHigh↑ Mitochondrial dysfunction, ↑ ROS, ↑ DNA damage—hallmarks of vascular ageing
[91]MixedChloroquineMiddle-aged mice + in vitro assaysSYRCLE + narrativeAttrition not fully reported; selective reporting in vitroSome concerns↑ Autophagy modulation; ↓ proteasome activity; lifespan extension in mice
[32]Mixed AcyclovirIn vivo (mouse) (male C57BL/6N mice, HFD + STZ-induced diabetes)
In vitro (HepG2) mechanistic
SYRCLE + narrativeRandom allocation to groups reported; small sample size; blinding and allocation concealment not clearly described; outcomes (glucose, lipids, oxidative stress) fully reported; no obvious selective reportingSome concerns/moderate↓ Fasting glucose, ↓ HbA1c, ↓ HOMA-IR; ↓ serum TG, T-CHO, LDL-C; ↑ hepatic T-SOD, ↓ MDA; ↑ glucose uptake in HepG2; ↓ ROS and AGEs; activation of PKM1 → AMPK/SIRT1 axis (metabolic/mitochondrial hallmarks relevant to vascular ageing)
[85]Mixed DHA (antimalarial/anti-infective)In vivo (rat fibrosis) + in vitro (HSC culture)Narrative + SYRCLELiver tissue (not vascular)
• Fibrosis model, not natural aging
• Drug regimen in pathological context, not typical antibiotic use
• No vascular cells/vascular function measured
Moderate relevance (mechanistic hypothesis)> 80% of p16+ cells were also p53+; < 9% Ki-67+ (implies senescence, not proliferation)
- DHA dose-dependently reduced collagen deposition/fibrosis area vs. fibrotic controls (p-values significant, exact values in original figures)
- In vitro, DHA increased G2/M-phase cells and decreased S-phase cells (quantitative shift vs. control)
- Upregulation of senescence markers (p53, p16, p21, HMGA1) and increased SA-β-gal positive cells after DHA
[146]MixedNitazoxanide (antiprotozoal/antiparasitic)Cell lines (senescence induced by bleomycin or D-galactose), and mice with bleomycin-induced pulmonary fibrosisNarrative + SYRCLEThe model is lung, not vascular tissue
• Fibrosis induced by chemical injury, not physiological aging
• No data on vascular cells or vascular remodeling
• Translational relevance to vascular aging inferred, not demonstrated
Moderate to high risk/indirect relevance↓ Senescence (fewer SA-β-gal + cells, preserved proliferation), ↓ SASP, preserved nuclear SIRT1, inhibited PI3K-WIPI1 pathway, attenuated fibrosis and collagen deposition in lungs

Tools applied included SYRCLE (animal), narrative appraisal (in vitro), or a combination. Ageing effects included mitochondrial dysfunction, autophagy modulation, senescence clearance, ROS induction, and immune-mediated removal of senescent cells (n = 6). : increased/upregulated/elevated, : decreased/downregulated/reduced. AMPK: AMP-activated protein kinase; DHA: dihydroartemisinin; HSC: hepatic stellate cell; MDA: malondialdehyde; PKM1: pyruvate kinase M1; ROS: reactive oxygen species; SASP: senescence-associated secretory phenotype; T-SOD: total superoxide dismutase.