ArticleMolecular medicine reports2020
2‑Hydroxypropyl‑β‑cyclodextrin blocks autophagy flux and triggers caspase‑8‑mediated apoptotic cascades in HepG2 cells.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed, 4 citations in OpenAlex.
- Cyclodextrins as Modulators of Regulated Cell Death: Implications for Immunometabolism and Therapeutic Innovation.Pharmaceutics · 2026Review
- Effects of Target of Rapamycin and Phosphatidylinositol 3-Kinase Inhibitors and Other Autophagy-Related Supplements on Life Span inInternational journal of molecular sciences · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cyclodextrin derivative, 2‑Hydroxypropyl-β‑cyclodextrin (HPβCD), from the cyclodextrin family is widely used as a drug carrier and offers promising strategies for treating neurodegenerative diseases and atherosclerosis regression. However, its side effects are not fully understood. Therefore, the aim of the present study was to investigate the possible adverse effects of relatively high concentrations of HPβCD on hepatocytes. It was found that a high dose (20 mM) of HPβCD treatment significantly inhibited the AKT/mTOR pathway and disrupted infusion of autophagosomes and lysosomes, which rapidly led to massive autophagosome accumulation in HepG2 cells. The autophagosomal membrane serves as a platform for caspase‑8 oligomerization, which is considered as the key step for its self‑activation. Using flow cytometry and TUNEL assay, increased apoptosis of HepG2 cells treated with a high dose HPβCD (20 mM) for 48 h was observed. In addition, western blotting results demonstrated that the expression of cleaved‑caspase‑8 was positively associated with microtubule‑associated protein 1 light chain 3 BII expression, which is an indicator of autophagosome level in the cytoplasm. Therefore, the present study provided novel evidence that HPβCD might be a potential risk contributing to the pathophysiological process of hepatic diseases, especially in an autophagy‑deficient state.
Indexed as
Identifiers
What OpenQuestion holds
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.