ArticlePloS one2013
AKIP1 expression modulates mitochondrial function in rat neonatal cardiomyocytes.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Assessing the Function of Porcine A Kinase-Interacting Protein 1 (AKIP1) In Vitro-A Central Regulator of Oxidative Stress and Mitochondrial Functions.International journal of molecular sciences · 2025Article
- Effect of Chronic Stress on Whole Blood Transcriptome: A Meta-Analysis of Publicly Available Datasets from Rodent Models.bioRxiv : the preprint server for biology · 2025Article
- Stroke-like lesion and status epilepticus in a child withFrontiers in neurology · 2025Article
- A Kinase Interacting Protein 1 regulates mitochondrial protein levels in energy metabolism and promotes mitochondrial turnover after exercise.Scientific reports · 2023Article
- A Kinase Interacting Protein 1 (AKIP1) promotes cardiomyocyte elongation and physiological cardiac remodelling.Scientific reports · 2023Article
- The erythropoietin receptor expressed in skeletal muscle is essential for mitochondrial biogenesis and physiological exercise.Pflugers Archiv : European journal of physiology · 2021Article
- The role of miR-320 in glucose and lipid metabolism disorder-associated diseases.International journal of biological sciences · 2021Review
- Article
- A-kinase interacting protein 1 (AKIP1) associates with advanced overall disease condition, tumor properties, and unfavorable prognosis in hepatocellular carcinoma patients.Journal of clinical laboratory analysis · 2020Article
- A-kinase-interacting protein 1 overexpression correlates with deteriorative tumor features and worse survival profiles, and promotes cell proliferation but represses apoptosis in non-small-cell lung cancer.Journal of clinical laboratory analysis · 2020Article
- AKIP1 promotes angiogenesis and tumor growth by upregulating CXC-chemokines in cervical cancer cells.Molecular and cellular biochemistry · 2018Article
- Does BCA3 Play a Role in the HIV-1 Replication Cycle?Viruses · 2018Article
- Establishment of a prediction model of changing trends in cardiac hypertrophy disease based on microarray data screening.Experimental and therapeutic medicine · 2016Article
- Overexpression of AKIP1 predicts poor prognosis of patients with breast carcinoma and promotes cancer metastasis through Akt/GSK-3β/Snail pathway.American journal of translational research · 2016Article
- Age Related Bioenergetics Profiles in Isolated Rat Cardiomyocytes Using Extracellular Flux Analyses.PloS one · 2016Article
- Impaired cardiac energy metabolism in embryos lacking adrenergic stimulation.American journal of physiology. Endocrinology and metabolism · 2015Article
- RhNRG-1β Protects the Myocardium against Irradiation-Induced Damage via the ErbB2-ERK-SIRT1 Signaling Pathway.PloS one · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A kinase interacting protein 1 (AKIP1) is a molecular regulator of protein kinase A and nuclear factor kappa B signalling. Recent evidence suggests AKIP1 is increased in response to cardiac stress, modulates acute ischemic stress response, and is localized to mitochondria in cardiomyocytes. The mitochondrial function of AKIP1 is, however, still elusive. Here, we investigated the mitochondrial function of AKIP1 in a neonatal cardiomyocyte model of phenylephrine (PE)-induced hypertrophy. Using a seahorse flux analyzer we show that PE stimulated the mitochondrial oxygen consumption rate (OCR) in cardiomyocytes. This was partially dependent on PE mediated AKIP1 induction, since silencing of AKIP1 attenuated the increase in OCR. Interestingly, AKIP1 overexpression alone was sufficient to stimulate mitochondrial OCR and in particular ATP-linked OCR. This was also true when pyruvate was used as a substrate, indicating that it was independent of glycolytic flux. The increase in OCR was independent of mitochondrial biogenesis, changes in ETC density or altered mitochondrial membrane potential. In fact, the respiratory flux was elevated per amount of ETC, possibly through enhanced ETC coupling. Furthermore, overexpression of AKIP1 reduced and silencing of AKIP1 increased mitochondrial superoxide production, suggesting that AKIP1 modulates the efficiency of electron flux through the ETC. Together, this suggests that AKIP1 overexpression improves mitochondrial function to enhance respiration without excess superoxide generation, thereby implicating a role for AKIP1 in mitochondrial stress adaptation. Upregulation of AKIP1 during different forms of cardiac stress may therefore be an adaptive mechanism to protect the heart.
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