Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Overexpression of Mitochondrial Transcription Factor A Ameliorates Mitochondrial Deficiencies and Cardiac Failure After Myocardial Infarction

26 Jul 2005

Abstract excerpt

BACKGROUND: Mitochondrial DNA (mtDNA) copy number is decreased not only in mtDNA-mutation diseases but also in a wide variety of acquired degenerative and ischemic diseases. Mitochondrial transcription factor A (TFAM) is essential for mtDNA transcription and replication. Myocardial mtDNA copy number and TFAM expression both decreased in cardiac failure. However, the functional significance of TFAM has not been...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cardiovascular Function and Risk Factors
Share to Congenital heart defects research
Share to Mitochondrial Function and Pathology

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 16043643
DOI: 10.1161/circulationaha.104.524835

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Overexpression of Mitochondrial Transcription Factor A Ameliorates Mitochondrial Deficiencies and Cardiac Failure After Myocardial InfarctionPMID 16043643Read ↗

Divergent Mitochondrial Biogenesis Responses in Human CardiomyopathySemantic proximity Read ↗

Decreased Peripheral Mitochondrial DNA Copy Number is Associated with the Risk of Heart Failure and Long-term OutcomesSemantic proximity Read ↗

Impaired mitochondrial biogenesis is a common feature to myocardial hypertrophy and end-stage ischemic heart failureSemantic proximity Read ↗

Increased CPT1a expression is a critical cardioprotective response to pathological stress that suppresses gene programs for remodeling and enables rescue by gene transferSemantic proximity Read ↗

Mitochondrial transcription factors TFAM and TFB2M regulate Serca2 gene transcription.Semantic proximity Read ↗

Mitochondrial transcription factor A is necessary for mtDNA maintenance and embryogenesis in mice.Semantic proximity Read ↗

ATPase Inhibitor Factor-1 Disrupts Mitochondrial Ca2+ Handling and Promotes Pathological Cardiac Hypertrophy through CaMKIIδSemantic proximity Read ↗

Defective DNA Replication Impairs Mitochondrial Biogenesis In Human Failing HeartsSemantic proximity Read ↗

Plasma nuclear and mitochondrial DNA levels in acute myocardial infarction patientsSemantic proximity Read ↗

Twinkle overexpression prevents cardiac rupture after myocardial infarction by alleviating impaired mitochondrial biogenesis.Semantic proximity Read ↗

Inhibiting Runx1 protects heart function after myocardial infarctionSemantic proximity Read ↗

Targeting DNA methylation can reduce cardiac injury associated with ischemia reperfusion: One step closer to clinical translation with blood-borne assessmentSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.