ReviewMolecular medicine reports2026
Targeting lipophagy in atherosclerosis: Molecular mechanisms, pathogenesis and therapeutic interventions (Review).
Review in Molecular medicine reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- Sphingolipid Metabolism: A Pathological Hub Linking Lipid Dysregulation and Chronic Inflammation in Atherosclerotic Cardiovascular Disease.Journal of inflammation research · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis (AS) is a chronic inflammatory disease characterized by lipid accumulation within the arterial wall. The imbalance between cholesterol influx and efflux, coupled with persistent inflammation, drives the progression of plaque formation. Lipophagy, a selective form of autophagy, specifically targets lipid droplets for lysosomal degradation. Consequently, this process is a notable regulator of cellular lipid homeostasis. In the present review, the core regulatory networks of lipophagy were systematically summarized, including the mechanistic target of rapamycin complex 1/AMP‑activated protein kinase, transcription factor EB (TFEB) and farnesoid X receptor/cAMP response element‑binding protein signaling axes. The multidimensional roles of lipophagy in key cell types involved in AS are also discussed. For example, in macrophages, lipophagy stabilizes plaques by promoting cholesterol efflux and inhibiting foam cell formation; however, dysregulated lipophagy can exacerbate necrotic core formation. In vascular smooth muscle cells, lipophagy regulates phenotype switching and calcification and in endothelial cells, lipophagy mitigates oxidative stress and inflammation. Advances in therapeutic strategies targeting lipophagy were evaluated, ranging from pharmacological agents (such as statins and metformin) to natural compounds (such as berberine and geniposide) and Traditional Chinese Medicine formulas. In conclusion, targeting lipophagy represents a pivotal therapeutic frontier for stabilizing atherosclerotic plaques; however, the broad application of autophagy inducers lacks precision. Future strategies should transition from generalized modulation to cell‑type specific interventions that precisely calibrate the sirtuin 1‑TFEB‑lipophagy axis. Furthermore, elucidating the 'double‑edged' role of lipophagy in late‑stage plaque outcomes is required for developing safe, clinically translatable modulators.
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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.