ArticleFrontiers in physiology2013
Mitochondrial NHE1: a newly identified target to prevent heart disease.
Article in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- TFEB Deficiency Impairs Male Fertility Through Mitochondrial Dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- NHE1-Mediated Metabolic Reprogramming in Cancer.Metabolites · 2026Review
- Merck Open Global Health Library in vitro screening against Schistosoma mansoni identified two new substances with antischistosomal activities for further development.Parasites & vectors · 2025Article
- The SGLT2 inhibitor empagliflozin improves cardiac energy status via mitochondrial ATP production in diabetic mice.Communications biology · 2023Article
- Emerging Therapy for Diabetic Cardiomyopathy: From Molecular Mechanism to Clinical Practice.Biomedicines · 2023Review
- Of mitochondrion and COVID-19.Journal of enzyme inhibition and medicinal chemistry · 2021Review
- Decoding empagliflozin's molecular mechanism of action in heart failure with preserved ejection fraction using artificial intelligence.Scientific reports · 2021Article
- The therapeutic importance of acid-base balance.Biochemical pharmacology · 2021Review
- Tracking intra- and inter-organelle signaling of mitochondria.The FEBS journal · 2019Review
- Voltage gated proton channels modulate mitochondrial reactive oxygen species production by complex I in renal medullary thick ascending limb.Redox biology · 2019Article
- (Patho-)Physiology of NaFrontiers in physiology · 2019Review
- miR-185 inhibits endoplasmic reticulum stress-induced apoptosis by targeting Na+/H+ exchanger-1 in the heart.BMB reports · 2016Article
- NHE1 deficiency in liver: implications for non-alcoholic fatty liver disease.Biochemical and biophysical research communications · 2014Article
- Mitochondria: the cell powerhouse and nexus of stress.Frontiers in physiology · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial damage has been associated with early steps of cardiac dysfunction in heart subjected to ischemic stress, oxidative stress and hypertrophy. A common feature for the mitochondrial deterioration is the loss of the mitochondrial membrane potential (ΔΨ m) with the concomitant irreversible opening of the mitochondrial permeability transition pore (MPTP) which follows the mitochondrial Ca(2+) overload, and the subsequent mitochondrial swelling. We have recently characterized the expression of the Na(+)/H(+) exchanger 1 (mNHE1) in mitochondrial membranes. This surprising observation provided a unique target for the prevention of the Ca(2+)-induced MPTP opening, based on the inhibition of the NHE1 m. In this line, inhibition of NHE1 m activity and/or reduction of NHE1 m expression decreased the Ca(2+)-induced mitochondrial swelling and the release of reactive oxygen species (ROS) in isolated cardiac mitochondria and preserved the ΔΨ m in isolated cardiomyocytes. Mitochondrial NHE1 thus represents a novel target to prevent cardiac disease, opening new avenues for future research.
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