Evidence map›Paper›PMID 37921069›Full record

ArticleMolecular medicine reports2023

IGF‑1 inhibits palmitic acid‑induced mitochondrial apoptosis in macrophages.

Wanying Tang, Ming Zhang, Yu Wang, Dan Ma, Mi Hu, Yangkai Zhang, Huiling Lin, Weiwei Jiang, Yuxin Ouyang, Liping Jiang and 3 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 32% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
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 at 6 institutions in 1 country.

Wanying Tang *Department of Physiology, Institute of Neuroscience Research, Hengyang Key Laboratory of Neurodegeneration and Cognitive Impairment, University of South China, Hengyang, Hunan 421001, P.R. China.
Ming Zhang *Institute of Cardiovascular Disease, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan, Guangdong 511500, P.R. China.
Yu WangInstitute of Cardiovascular Disease, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan, Guangdong 511500, P.R. China.
Dan MaSchool of Pharmacy Zunyi Medical University, Zunyi, Guizhou 563000, P.R. China.
Mi HuDepartment of Physiology, Institute of Neuroscience Research, Hengyang Key Laboratory of Neurodegeneration and Cognitive Impairment, University of South China, Hengyang, Hunan 421001, P.R. China.
Yangkai ZhangDepartment of Physiology, Institute of Neuroscience Research, Hengyang Key Laboratory of Neurodegeneration and Cognitive Impairment, University of South China, Hengyang, Hunan 421001, P.R. China.
Huiling LinDepartment of Physiology, Institute of Neuroscience Research, Hengyang Key Laboratory of Neurodegeneration and Cognitive Impairment, University of South China, Hengyang, Hunan 421001, P.R. China.
Weiwei JiangDepartment of Organ Transplantation, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, P.R. China.
Yuxin OuyangDepartment of Physiology, Institute of Neuroscience Research, Hengyang Key Laboratory of Neurodegeneration and Cognitive Impairment, University of South China, Hengyang, Hunan 421001, P.R. China.
Liping JiangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Pingping HeThe Research Center of Reproduction and Translational Medicine of Hunan Province, Department of Physiology, Medical College, Hunan Normal University, Changsha, Hunan 410081, P.R. China.
Guojun ZhaoInstitute of Cardiovascular Disease, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan, Guangdong 511500, P.R. China.
Xinping OuyangDepartment of Physiology, Institute of Neuroscience Research, Hengyang Key Laboratory of Neurodegeneration and Cognitive Impairment, University of South China, Hengyang, Hunan 421001, P.R. China.
University of South China · CNGuangzhou Medical University · CNCentral South University · CNHunan Normal University · CNSouthern Medical University · CNZunyi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin growth factor‑1 (IGF‑1) is an endocrine regulator that plays an important role in normal growth and development. IGF‑1 mediated effects may result in protecting macrophages from immunometabolic response. However, it is unclear whether IGF‑1 has a protective effect on fatty acid‑induced macrophages damage. In the present study, THP‑1 cells were differentiated into macrophages and stimulated with palmitic acid (PA) in the absence or presence of IGF‑1. Macrophages apoptosis was measured by Cell Counting Kit‑8 assay, flow cytometry, Hoechst 33342 staining and western blotting. The mitochondrial damage was evaluated using JC‑1 staining and mitochondrial reactive oxygen species detection. The activation of mitophagy was assessed using immunofluorescence and western blotting. As a result, IGF‑1 significantly restored the survival rate in macrophages, while the apoptosis was inhibited through mitochondrial pathway. In addition, IGF‑1 protected the mitochondrial damage induced by PA. Furthermore, PA induced mitophagy via phosphatase and tensin homolog‑induced putative kinase protein 1/Parkin, which was reversed by IGF‑1. Taken together, the present study demonstrated the protective effect of IGF‑1 on PA‑induced mitochondrial apoptosis in macrophages, which might provide a potential therapeutic strategy for treatment of lipotoxicity.

Indexed as

InsulinPalmitic AcidApoptosisInsulin-Like Growth Factor IMitophagyReactive Oxygen SpeciesUbiquitin-Protein LigasesInsulinInsulin-Like Growth Factor IPalmitic AcidReactive Oxygen SpeciesUbiquitin-Protein Ligasesapoptosisinsulin growth factormacrophagesmitochondriapalmitic acid

Identifiers

PMID37921069
PMCPMC10636768
OpenAlexW4388140082

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.