LncRNA MIAT knockdown alleviates oxygen-glucose deprivation‑induced cardiomyocyte injury by regulating JAK2/STAT3 pathway via miR-181a-5p.

Background: Coronary artery disease (CAD) is a common heart disease with high incidence and mortality. Myocardial ischemia is the main type of CAD, which negatively affects health worldwide. The aim of the present study was to investigate the function and mechanism of myocardial infarction-associated transcript (MIAT) in myocardial ischemia.

Antioxidant defence system is responsible for the toxicological interactions of mixtures: A case study on PFOS and PFOA in Daphnia magna.

Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are two types of perfluorinated compounds (PFCs) frequently studied in recent years due to their potential for bioaccumulation and toxicity to humans. Usually, PFCs can co-exist in various environment. Therefore, over- or under-estimated risk assessments would result if antagonism or synergism occurred in mixture toxicity.

NFATc4 and myocardin synergistically up-regulate the expression of LTCC α1C in ET-1-induced cardiomyocyte hypertrophy.

Aims: Dysregulation of Ca(2+) is a central cause of cardiac hypertrophy. The α1C subunit of L-type Ca(2+) channel (LTCC) is a pore-forming protein which is responsible for the voltage-dependent channel gating and channel selectivity for Ca(2+). Myocardin and nuclear factor of activated T-cells c4 (NFATc4) are two key transcription factors in cardiac hypertrophy.

MicroRNA-29a-3p attenuates ET-1-induced hypertrophic responses in H9c2 cardiomyocytes.

Transcription factor nuclear factor of activated T cells c4 (NFATc4) is the best-characterized target for the development of cardiac hypertrophy. Aberrant microRNA-29 (miR-29) expression is involved in the development of cardiac fibrosis and congestive heart failure. However, whether miR-29 regulates hypertrophic processes is still not clear.

Ca²⁺ signal-induced cardiomyocyte hypertrophy through activation of myocardin.

Hypertrophic growth of cardiomyocytes in response to pressure overload is an important stage during the development of many cardiac diseases. Ca(2+) overload as well as subsequent activation of Ca(2+) signaling pathways has been reported to induce cardiac hypertrophy. Myocardin, a transcription cofactor of serum response factor (SRF), is a key transducer of hypertrophic signals.