Dioscin elevates lncRNA MANTIS in therapeutic angiogenesis for heart diseases

Abstract

The major function of the circulatory system is to deliver oxygen and nutrients to the cells throughout body (Del Re et al., 2019;Kaelin et al., 2016). An insufficient blood supply, if not corrected in time, leads to depletion of oxygen and nutrients to vital organs, resulting in organ failure and death. As we know, coronary artery disease (CAD) and stroke caused by ischemia, a sudden and severe blockage of coronary or brain arteries, are one of the most common causes of death worldwide (Khera & Kathiresan, 2017;Vogel et al., 2019).Every year, an estimation of 720,000 people in the United States is hospitalized with acute coronary syndrome or has fatal coronary heart disease events (Rodriguez & Harrington, 2021).Myocardial infarction (MI) is the most severe manifestation of CAD. Approximately every 40 s, an individual is hospitalized due to myocardial infarction (van Diepen et al., 2017). Reperfusion strategies, including angiography and percutaneous coronary intervention (PCI), are the widely used for CAD and MI patients (Thiele et al., 2018). Also, artery bypass graft surgery is considered to treat MI patients with a large myocardial area at jeopardy or cardiogenic shock (Solo et al., 2019). However, these therapeutic strategies are not suitable for some elder patients with diffuse myocardial infarction. To meet the needs

Dioscin ameliorates doxorubicin‐induced heart failure via inhibiting autophagy and apoptosis by controlling the PDK1‐mediated Akt/mTOR signaling pathway

“…28 It was implied by Kong that Dioscin alleviated hypoxic-caused cardiac dysfunction in myocardial infarction via elevating the level of lncRNA MANTIS. 29 Dioscin improved myocardial infarction damage through adjusting BMP4/NOX1-mediated inflammation. 30 In addition, Dox was reported as an effective and commonly used to treat hematological and solid tumors.…”

Roles of Epigenetics in Cardiac Fibroblast Activation and Fibrosis

“…LncRNA Crnde also suppresses CFs activation and alleviates DCM-associated cardiac fibrosis through negative feedback regulation of Smad3 transcriptional activation [ 145 ]. Dioscin, a glucoside saponin isolated from Dioscorea nipponica Makino , reduced MI-induced cardiac fibrosis by upregulating lncRNA MANTIS to promote the expression of angiogenesis-related genes such as SOX18, SMAD6, and COUP-TFII [ 146 ]. Meanwhile, histone demethylase JARID1B could also regulate lncRNA MANTIS and restrict the expression of angiogenesis-related genes such as SMAD6 [ 153 ].…”

Dioscin Alleviates Cardiac Dysfunction in Acute Myocardial Infarction via Rescuing Mitochondrial Malfunction

“…The protective effects are associated with mitochondrial function, including alleviating mitochondrial oxidative stress, de-activation of respiratory chain enzymes, postponing mitochondrial Kreb's cycle, and maintenance of mitochondrial membrane potential ( ψ) and ATP content (8)(9)(10). Dioscin, a natural steroid saponin isolated from the root bark of wild dioscorea nipponica, is reported to treat MI by promoting angiogenesis (11). Additionally, it was reported that dioscin maintains mitochondrial dynamics, which rescues silicosis by reducing mitochondrial-dependent apoptosis (12).…”

“…Taken together, our results showed that dioscin could alleviate MI via attenuate mitochondrial malfunction. Infarction mouse model was generated through ligature of the left anterior descending (LAD) as described previously with male mice (11). Briefly, mice were anesthetized with 1.5-2% isoflurane, and then a left thoracotomy and pericardiotomy was performed.…”