Ferroptosis Involved in Cardiovascular Diseases: Mechanism Exploration of Ferroptosis' Role in Common Pathological Changes.

ABSTRACT: Regulated cell death is a controlled form of cell death that protects cells by adaptive responses in pathophysiological states. Ferroptosis has been identified as a novel method of controlling cell death in recent years. Several cardiovascular diseases (CVDs) are shown to be profoundly influenced by ferroptosis, and ferroptosis is directly linked to the majority of cardiovascular pathological alterations. Despite this, it is still unclear how ferroptosis affects the pathogenic alterations that take place in CVDs. Based on a review of the mechanisms that regulate ferroptosis, this review explores the most recent research on the role of ferroptosis in the major pathological changes associated with CVDs, to provide new perspectives and strategies for cardiovascular research and clinical treatment.

Finding New Targets for the Treatment of Heart Failure: Endoplasmic Reticulum Stress and Autophagy.

Heart failure is a progressive disease with an annual mortality rate of about 10% and is the end-stage stage of various heart diseases, which places a huge socioeconomic burden on the healthcare system. The development of heart failure has received increasing attention as a potential way to improve the treatment of this disease. Many studies have shown that endoplasmic reticulum stress and autophagy play an important role in the occurrence and development of heart failure. With the in-depth study of endoplasmic reticulum stress and autophagy, both are considered promising targets for pharmacological interventions to treat heart failure, but the mechanism of heart failure between the two is not clear. This review will highlight the effects of endoplasmic reticulum stress, autophagy, and their interactions in the development and development of heart failure, thereby helping to provide direction for the future development of targeted therapies for patients with heart failure. CLINICAL RELEVANCE: This study explored the new targets for the treatment of heart failure: endoplasmic reticulum stress and autophagy. Targeted drug therapy for endoplasmic reticulum stress and autophagy is expected to provide a new intervention target for the treatment of heart failure.

From Iron Metabolism to Ferroptosis: Pathologic Changes in Coronary Heart Disease.

Coronary heart disease (CHD) is closely related to oxidative stress and inflammatory response and is the most common cardiovascular disease (CVD). Iron is an essential mineral that participates in many physiological and biochemical reactions in the human body. Meanwhile, on the negative side, iron has an active redox capacity, which leads to the accumulation of reactive oxygen species (ROS) and lipid peroxidation. There is growing evidence that disordered iron metabolism is involved in CHD's pathological progression. And the result of disordered iron metabolism is associated with iron overload-induced programmed cell death, often called ferroptosis. That features iron-dependent lipid peroxidation. Ferroptosis may play a crucial role in the development of CHD, and targeting ferroptosis may be a promising option for treating CHD. Here, we review the mechanisms of iron metabolism in cardiomyocytes (CMs) and explain the correlation between iron metabolism and ferroptosis. Meanwhile, we highlight the specific roles of iron metabolism and ferroptosis in the main pathological progression of CHD.

Mesenchymal Stem Cell Immunomodulation: A Novel Intervention Mechanism in Cardiovascular Disease.

Mesenchymal stem cells (MSCs) are the member of multipotency stem cells, which possess the capacity for self-renewal and multi-directional differentiation, and have several characteristics, including multi-lineage differentiation potential and immune regulation, which make them a promising source for cell therapy in inflammation, immune diseases, and organ transplantation. In recent years, MSCs have been described as a novel therapeutic strategy for the treatment of cardiovascular diseases because they are potent modulators of immune system with the ability to modulating immune cell subsets, coordinating local and systemic innate and adaptive immune responses, thereby enabling the formation of a stable inflammatory microenvironment in damaged cardiac tissues. In this review, the immunoregulatory characteristics and potential mechanisms of MSCs are sorted out, the effect of these MSCs on immune cells is emphasized, and finally the application of this mechanism in the treatment of cardiovascular diseases is described to provide help for clinical application.

Self-reporting Arabidopsis expressing pH and [Ca2+] indicators unveil ion dynamics in the cytoplasm and in the apoplast under abiotic stress.

For noninvasive in vivo measurements of intra- and extracellular ion concentrations, we produced transgenic Arabidopsis expressing pH and calcium indicators in the cytoplasm and in the apoplast. Ratiometric pH-sensitive derivatives of the green fluorescent protein (At-pHluorins) were used as pH indicators. For measurements of calcium ([Ca(2+)]), luminescent aequorin variants were expressed in fusion with pHluorins. An Arabidopsis chitinase signal sequence was used to deliver the indicator complex to the apoplast. Responses of pH and [Ca(2+)] in the apoplast and in the cytoplasm were studied under salt and "drought" (mannitol) stress. Results are discussed in the frame of ion flux, regulation, and signaling. They suggest that osmotic stress and salt stress are differently sensed, compiled, and processed in plant cells.