Evidence mapPaperPMID 41019998Full record

ArticleFrontiers in pharmacology2025

Improved myocardial mitochondrial energy metabolism in rats with chronic heart failure by modifying fatty acid oxidation using an extract of sand-fired aconite (Jianchang gang processing).

Hongtao Zhang, Yi Huang, Songhong Yang, Feipeng Gong, Yuncheng Gu, Qin Xie, Yanrong Ye, Xingmei Lu, Lingyun Zhong

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Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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.

2 · The registry

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Hongtao ZhangSchool of Pharmacy, Jiangxi University of Chinese Medicine, Nanchang, China.
Yi HuangSchool of Pharmacy, Jiangxi University of Chinese Medicine, Nanchang, China.
Songhong YangSchool of Pharmacy, Jiangxi University of Chinese Medicine, Nanchang, China.
Feipeng GongJiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.
Yuncheng GuJiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.
Qin XieSchool of Pharmacy, Jiangxi University of Chinese Medicine, Nanchang, China.
Yanrong YeSchool of Pharmacy, Jiangxi University of Chinese Medicine, Nanchang, China.
Xingmei LuSchool of Pharmacy, Jiangxi University of Chinese Medicine, Nanchang, China.
Lingyun ZhongSchool of Pharmacy, Jiangxi University of Chinese Medicine, Nanchang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Sand-fired aconite slices (SFAS) demonstrate anti-heart failure effects, but the mechanism remains unclear. This study investigated myocardial mitochondrial energy metabolism as a therapeutic mechanism of SFAS in doxorubicin-induced chronic heart failure (CHF) rats. Methods: The CHF rat model was established via the intraperitoneal injection of doxorubicin (DOX). Following successful model production, rats were randomly assigned to nine groups. After drug administration, their cardiac function was assessed, and their cardiac tissue morphology and myocardial mitochondria were examined. Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), norepinephrine (NE), malondialdehyde (MDA), superoxide dismutase (SOD), free fatty acid (FFA), sodium-potassium-ATPase (Na Results: SFAS significantly improved cardiac function in CHF rats. It increased the left ventricular ejection fraction (LVEF) (from 34.22% ± 2.03%-83.68% ± 2.34%; Conclusion: By activating the AMPK/PGC-1α/SIRT3 signaling pathway, SFAS ameliorated the impaired fatty acid oxidation pathway and enhanced mitochondrial function and antioxidant capacity in cardiomyocytes, ultimately reducing myocardial damage and restoring cardiac function in CHF rats.

Indexed as

chronic heart failureenergy metabolismfatty acidmitochondriaoxidative stresssand fired aconite slices

Identifiers

PMID41019998
PMCPMC12461213

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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 Socratic graph.