Evidence map›Paper›PMID 34777380›Full record

ReviewFrontiers in immunology2021

The Role of HDAC6 in Autophagy and NLRP3 Inflammasome.

Panpan Chang, Hao Li, Hui Hu, Yongqing Li, Tianbing Wang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.3field-weighted citation impact, top 4% of its field
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

53 citing papers in PubMed, 89 citations in OpenAlex.

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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

5 authors at 5 institutions in 2 countries.

Panpan ChangTrauma Medicine Center, Peking University People's Hospital, Key Laboratory of Trauma and Neural Regeneration (Peking University), National Center for Trauma Medicine of China, Beijing, China.
Hao LiDepartment of Emergency, First Hospital of China Medical University, Shenyang, China.
Hui HuDepartment of Traumatology, Central Hospital of Chongqing University, Chongqing Emergency Medical Center, Chongqing, China.
Yongqing LiDepartment of Surgery, University of Michigan, Ann Arbor, MI, United States.
Tianbing WangTrauma Medicine Center, Peking University People's Hospital, Key Laboratory of Trauma and Neural Regeneration (Peking University), National Center for Trauma Medicine of China, Beijing, China.
Chongqing University · CNFirst Hospital of China Medical University · CNPeking University · CNPeking University People's Hospital · CNUniversity of Michigan–Ann Arbor · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy fights against harmful stimuli and degrades cytosolic macromolecules, organelles, and intracellular pathogens. Autophagy dysfunction is associated with many diseases, including infectious and inflammatory diseases. Recent studies have identified the critical role of the NACHT, LRR, and PYD domain-containing protein 3 (NLRP3) inflammasomes activation in the innate immune system, which mediates the secretion of proinflammatory cytokines IL-1β/IL-18 and cleaves Gasdermin D to induce pyroptosis in response to pathogenic and sterile stimuli. Accumulating evidence has highlighted the crosstalk between autophagy and NLRP3 inflammasome in multifaceted ways to influence host defense and inflammation. However, the underlying mechanisms require further clarification. Histone deacetylase 6 (HDAC6) is a class IIb deacetylase among the 18 mammalian HDACs, which mainly localizes in the cytoplasm. It is involved in two functional deacetylase domains and a ubiquitin-binding zinc finger domain (ZnF-BUZ). Due to its unique structure, HDAC6 regulates various physiological processes, including autophagy and NLRP3 inflammasome, and may play a role in the crosstalk between them. In this review, we provide insight into the mechanisms by which HDAC6 regulates autophagy and NLRP3 inflammasome and we explored the possibility and challenges of HDAC6 in the crosstalk between autophagy and NLRP3 inflammasome. Finally, we discuss HDAC6 inhibitors as a potential therapeutic approach targeting either autophagy or NLRP3 inflammasome as an anti-inflammatory strategy, although further clarification is required regarding their crosstalk.

Indexed as

AutophagyHistone Deacetylase 6HumansInflammasomesMitophagyNLR Family, Pyrin Domain-Containing 3 ProteinHistone Deacetylase 6InflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinautophagyHDAC6inflammationNLRP3 inflammasomepost-translational modification

Identifiers

PMID34777380
PMCPMC8578992
OpenAlexW3210927346

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.