Evidence map›Paper›PMID 34386317›Full record

ReviewActa pharmaceutica Sinica. B2021

Natural compounds modulate the autophagy with potential implication of stroke.

Anil Ahsan, Mengru Liu, Yanrong Zheng, Wenping Yan, Lin Pan, Yue Li, Shijia Ma, Xingxian Zhang, Ming Cao, Zhanxun Wu and 3 more

Abstract readReview
In one paragraph

Review in Acta pharmaceutica Sinica. B, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 4 pooled it
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  5. Article
  6. Review
  7. Crosstalk between autophagy and ferroptosis in liver diseases (Review).International journal of molecular medicine · 2026
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  9. Article
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  15. Dichloromethane Extract fromAntioxidants (Basel, Switzerland) · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Anil AhsanInstitute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University, Hangzhou 310058, China.
Mengru LiuInstitute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University, Hangzhou 310058, China.
Yanrong ZhengInstitute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University, Hangzhou 310058, China.
Wenping YanInstitute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University, Hangzhou 310058, China.
Lin PanInstitute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University, Hangzhou 310058, China.
Yue LiInstitute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University, Hangzhou 310058, China.
Shijia MaInstitute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University, Hangzhou 310058, China.
Xingxian ZhangInstitute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University, Hangzhou 310058, China.
Ming CaoInstitute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University, Hangzhou 310058, China.
Zhanxun WuInstitute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University, Hangzhou 310058, China.
Weiwei HuInstitute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University, Hangzhou 310058, China.
Zhong ChenInstitute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University, Hangzhou 310058, China.
Xiangnan ZhangInstitute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University, Hangzhou 310058, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke is considered a leading cause of mortality and neurological disability, which puts a huge burden on individuals and the community. To date, effective therapy for stroke has been limited by its complex pathological mechanisms. Autophagy refers to an intracellular degrading process with the involvement of lysosomes. Autophagy plays a critical role in maintaining the homeostasis and survival of cells by eliminating damaged or non-essential cellular constituents. Increasing evidence support that autophagy protects neuronal cells from ischemic injury. However, under certain circumstances, autophagy activation induces cell death and aggravates ischemic brain injury. Diverse naturally derived compounds have been found to modulate autophagy and exert neuroprotection against stroke. In the present work, we have reviewed recent advances in naturally derived compounds that regulate autophagy and discussed their potential application in stroke treatment.

Indexed as

AD, Alzheimer's diseaseALS, amyotrophic lateral sclerosisAMPK, 5′-adenosine monophosphate-activated protein kinaseATF6, activating transcription factor 6ATG, autophagy related genesAutophagyBCL-2, B-cell lymphoma 2BNIP3L, BCL2/adenovirusCerebral ischemiaCOPII, coat protein complex IIeIF2a, eukaryotic translation-initiation factor 2ER, endoplasmic reticulumFOXO, forkhead box OFUNDC1, FUN14 domain containing 1GPCR, G-protein coupled receptorHD, Huntington's diseaseIPC, ischemic preconditioningIRE1, inositol-requiring enzyme 1JNK, c-Jun N-terminal kinaseLAMP, lysosomal-associated membrane proteinLC3, light chain 3LKB1, liver kinase B1Lysosomal activationMitochondriaMitophagymTOR, mechanistic target of rapamycinNatural compoundsNeurological disordersNeuroprotectionOGD/R, oxygen and glucose deprivation-reperfusionPD, Parkinson's diseasePERK, protein kinase R (PKR)-like endoplasmic reticulum kinasePI3K, phosphatidylinositol 3-kinaseROS, reactive oxygen speciesSQSTM1, sequestosome 1TFEB, transcription factor EBTIGAR, TP53-induced glycolysis and apoptosis regulatorULK, Unc-51- like kinaseUro-A, urolithin AΔΨm, mitochondrial membrane potential

Identifiers

PMID34386317
PMCPMC8343111

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Registered trials

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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.