Evidence map›Paper›PMID 31388827›Full record

ArticleCell stress & chaperones2019

Tanshinone IIA attenuates cardiac microvascular ischemia-reperfusion injury via regulating the SIRT1-PGC1α-mitochondrial apoptosis pathway.

Jiankai Zhong, Haichun Ouyang, Mingming Sun, Jianhua Lu, Yuanlin Zhong, Ying Tan, Yunzhao Hu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell stress & chaperones, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
6.1field-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

26 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
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  4. Role of natural products in cardiovascular disease.Molecular and cellular biochemistry · 2025
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  7. Review
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  10. The role and mechanisms of microvascular damage in the ischemic myocardium.Cellular and molecular life sciences : CMLS · 2023
    Review
  11. Article
  12. Review
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  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
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  20. 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

7 authors at 4 institutions in 2 countries.

Jiankai ZhongDepartment of Cardiology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, 528300, Guangdong, China.
Haichun OuyangDepartment of Cardiology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, 528300, Guangdong, China.
Mingming SunDepartment of Animal Science, University of Wyoming, Laramie, WY, 82071, USA.
Jianhua LuDepartment of Cardiology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, 528300, Guangdong, China.
Yuanlin ZhongDepartment of Cardiology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, 528300, Guangdong, China.
Ying TanDepartment of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. tanying1115@163.com.
Yunzhao HuDepartment of Cardiology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, 528300, Guangdong, China. sdhuyz@163.com.
Southern Medical University · CNNanfang Hospital · CNThe First People's Hospital of Shunde · CNUniversity of Wyoming · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac microvascular ischemia-reperfusion (IR) injury has been a neglected topic in recent decades. In the current study, we investigated the mechanism underlying microvascular IR injury, with a focus on mitochondrial homeostasis. We also explored the protective role of tanshinone IIA (Tan IIA) in microvascular protection in the context of IR injury. Through animal studies and cell experiments, we demonstrated that IR injury mediated microvascular wall destruction, lumen stenosis, perfusion defects, and cardiac microvascular endothelial cell (CMEC) apoptosis via inducing mitochondrial damage. In contrast, Tan IIA administration had the ability to sustain CMEC viability and microvascular homeostasis, finally attenuating microvascular IR injury. Function studies have confirmed that the SIRT1/PGC1α pathway is responsible for the microvascular protection from the Tan IIA treatment. SIRT1 activation by Tan IIA sustained the mitochondrial potential, alleviated the mitochondrial pro-apoptotic factor leakage, reduced the mPTP opening, and blocked mitochondrial apoptosis, providing a survival advantage for CMECs and preserving microvascular structure and function. By comparison, inhibiting SIRT1 abrogated the beneficial effects of Tan IIA on mitochondrial function, CMEC survival, and microvascular homeostasis. Collectively, this study indicated that Tan IIA should be considered a microvascular-protective drug that alleviates acute cardiac microcirculation IR injury via activating the SIRT1/PGC1α pathway and thereby blocking mitochondrial damage.

Indexed as

AbietanesAnimalsApoptosisEndothelial CellsHeartMiceMice, Inbred C57BLMitochondriaMyocardial Reperfusion InjuryPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaSirtuin 1AbietanesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseSirt1 protein, mouseSirtuin 1tanshinoneCardiac microvascular IR injuryCMECMitochondrial apoptosisSIRT1/PGC1α pathwaysTan IIA

Identifiers

PMID31388827
PMCPMC6717231
OpenAlexW2965404232

What OpenQuestion holds

Textmetadata
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.