ReviewChinese medical journal2026
Regulation of mitochondrial biogenesis and energy metabolism in the heart.
Review in Chinese medical journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Ailanthone as a novel AKT1 inhibitor that induces mitochondrial apoptosis and exerts anti-tumor activity in cervical cancer.Translational cancer research · 2026Article
- EGCG-Functionalized Selenium Nanoparticles Mitigate High-Fat Diet-Induced Hepatic Lipotoxicity Through Keap1/Nrf2 Redox Modulation and Transcriptional Regulation of AMPK/SIRT1/PGC-1α/MFN2-Associated Mitochondrial Homeostasis.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractMitochondrial homeostasis is regulated by processes such as biogenesis, dynamics, and mitophagy, and is essential for maintaining cardiac function while preserving structural integrity, energy supply, and redox balance. Given their high reliance on mitochondrial adenosine triphosphate generation, cardiomyocytes are particularly vulnerable to mitochondrial dysfunction. In the cardiovascular system, mitochondria respond to various pathophysiological conditions, such as ischemia-reperfusion injury, hypertension, diabetic cardiomyopathy, and heart failure. Mitochondrial impairment drives cardiovascular disease progression through deficient energy production, elevated oxidative stress, activation of inflammatory responses, and programmed cell death. Growing evidence highlights the critical roles of epigenetic and transcriptional networks in the coordinated regulation of mitochondrial biogenesis and metabolism. Targeting these processes is a promising therapeutic strategy to improve mitochondrial health in cardiovascular diseases. This review systematically summarizes recent advances, outlines the key regulatory mechanisms of mitochondrial biogenesis and metabolism, and explores their pathophysiological roles and therapeutic potential.
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Identifiers
What OpenQuestion holds
Registered trials
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.