Silencing N29 Regulated miR-193b-5p/TGFBR2 Axis to Mitigate the Progression of Cardiac Hypertrophy.

The study aimed to analyze differentially expressed lncRNAs in a model of cardiac hypertrophy, specially focusing on the molecular mechanisms of lncRNA NONMMUT023529 (lncRNA N29) in myocardial hypertrophy. Based on gene microarray results, RT-qPCR validation confirmed that lncRNA N29 was significantly upregulated in TAC-induced mice cardiac tissues. Echocardiographic assessments further verified that silencing lncRNA N29 led to a marked improvement in cardiac function, which aligned with the pathological findings revealed by H&E and Masson staining.

Endoplasmic reticulum stress-mediated cell death in cardiovascular disease.

The endoplasmic reticulum (ER) plays a vital function in maintaining cellular homeostasis. Endoplasmic reticulum stress (ERS) can trigger various modes of cell death by activating the unfolded protein response (UPR) signaling pathway. Cell death plays a crucial role in the occurrence and development of diseases such as cancer, liver diseases, neurological diseases, and cardiovascular diseases.

Knockdown of microglial Cav2.2 N-type voltage-dependent Ca channel ameliorates behavioral deficits in a mouse model of Parkinson's disease.

Cav2.2 N-type voltage-dependent Ca channel (VDCC) expressed in neurons is known to be essential for neurotransmitter release. We have shown previously that this channel is also expressed in nonexcitable microglia and plays pivotal roles in microglial functions.

Involvement of N-type Ca channel in microglial activation and its implications to aging-induced exaggerated cytokine response.

Voltage-dependent calcium channel (VDCC) is generally believed to be active only in excitable cells. However, we have reported recently that N-type VDCC (Cav2.2) could become functional in non-excitable cells under pathological conditions.

Blockade of microglial Cav1.2 Ca channel exacerbates the symptoms in a Parkinson's disease model.

Cav1.2 channels are an L-type voltage-dependent Ca channel, which is specifically blocked by calcium antagonists. Voltage-dependent Ca channels are generally considered to be functional only in excitable cells like neurons and muscle cells, but recently they have been reported to also be functional in non-excitable cells like microglia, which are key players in the innate immune system and have been shown to be involved in the pathophysiology of Parkinson's disease.