ReviewBioMed research international2020
The Role of Autophagy and NLRP3 Inflammasome in Liver Fibrosis.
Review in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 73 citations in OpenAlex.
- From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis.Liver research (Beijing, China) · 2026Review
- 3-carbamoyl proxyl nitroxide attenuates CClScientific reports · 2026Article
- Diacerein improves liver fibrosis, steatosis, and atherosclerosis in ApoE knockout mice.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Luteolin and its derivatives: modulation of epithelial-mesenchymal transition in fibrosis and cancer.Frontiers in pharmacology · 2026Review
- Protective anti-fibrotic effect of liraglutide and Pirfenidone combination therapy on liver fibrosis in rats: effects on autophagy and NLRP3 inflammasome.BMC gastroenterology · 2025Article
- Unravelling the reversion mechanisms of activated hepatic stellate cell properties by extracellular vesicles from mesenchymal stem cells.World journal of stem cells · 2025Review
- PROM2 exacerbates CCl4-Induced liver fibrosis via NLRP3 inflammasome activation and hepatocyte pyroptosis.Cellular and molecular life sciences : CMLS · 2025Article
- Rev‑erbα: The circadian guardian against NLRP3‑driven liver fibrosis.Molecular medicine reports · 2025Article
- The Protective Role of Baicalin in the Regulation of NLRP3 Inflammasome in Different Diseases.Cell biochemistry and biophysics · 2025Review
- SLC26A4 regulates autophagy and activates the NLRP3 inflammasome to mediate pathological cardiac hypertrophy.Scientific reports · 2025Article
- Targeting SIRT2 in Aging-Associated Fibrosis Pathophysiology.Aging and disease · 2024Review
- The hepatoprotective effect of 4-phenyltetrahydroquinolines on carbon tetrachloride induced hepatotoxicity in rats through autophagy inhibition.Biological research · 2024Article
- Progress in the Correlation Between Inflammasome NLRP3 and Liver Fibrosis.Journal of clinical and translational hepatology · 2024Review
- Mechanisms and effects of NLRP3 in digestive cancers.Cell death discovery · 2024Review
- The molecular mechanism of MiR-26a-5p regulates autophagy and activates NLRP3 inflammasome to mediate cardiomyocyte hypertrophy.BMC cardiovascular disorders · 2024Article
- Hepatic NLRP3-Derived Hsp70 Binding to TLR4 Mediates MASLD to MASH Progression upon Inhibition of PP2A by Harmful Algal Bloom Toxin Microcystin, a Second Hit.International journal of molecular sciences · 2023Article
- Angiotensin-converting enzyme 2 improves liver fibrosis in mice by regulating autophagy of hepatic stellate cells.World journal of gastroenterology · 2023Article
- PTEN Overexpression Alters Autophagy Levels and Slows Sodium Arsenite-Induced Hepatic Stellate Cell Fibrosis.Toxics · 2023Article
- Liver Fibrosis Resolution: From Molecular Mechanisms to Therapeutic Opportunities.International journal of molecular sciences · 2023Review
- SEMtree: tree-based structure learning methods with structural equation models.Bioinformatics (Oxford, England) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis is an intrinsic repair process of chronic injury with excessive deposition of extracellular matrix. As an early stage of various liver diseases, liver fibrosis is a reversible pathological process. Therefore, if not being controlled in time, liver fibrosis will evolve into cirrhosis, liver failure, and liver cancer. It has been demonstrated that hepatic stellate cells (HSCs) play a crucial role in the formation of liver fibrosis. In particular, the activation of HSCs is a key step for liver fibrosis. Recent researches have suggested that autophagy and inflammasome have biological effect on HSC activation. Herein, we review current studies about the impact of autophagy and NOD-like receptors containing pyrin domain 3 (NLRP3) inflammasome on liver fibrosis and the underlying mechanisms.
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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.