Epac: A Promising Therapeutic Target for Vascular Diseases: A Review

Pan, Yuwei; Liu, Jia; Ren, Jiahui; Luo, Yun; Sun, Xiaobo

doi:10.3389/fphar.2022.929152

Cited by 4 publications

(2 citation statements)

References 143 publications

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“…Consequently, PKA inhibits the GSK3, PI3K/Akt and NF-κB pathways ( 191 ). Stimulated Epac1/2 promotes the activation of SOCS3 via the stimulation of RAP1, c-Jun, and C/EBPβ ( 192 ). At the same time, cAMP-stimulated Epac1/2 also inhibits the NF-κB- and GSK3β-mediated pro-inflammatory cytokine production ( 193 ).…”

Section: Comparison Of Ramp- and Damp-induced Signaling Pathways On P...mentioning

confidence: 99%

Damage-mediated macrophage polarization in sterile inflammation

et al. 2023

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Most of the leading causes of death, such as cardiovascular diseases, cancer, dementia, neurodegenerative diseases, and many more, are associated with sterile inflammation, either as a cause or a consequence of these conditions. The ability to control the progression of inflammation toward tissue resolution before it becomes chronic holds significant clinical potential. During sterile inflammation, the initiation of inflammation occurs through damage-associated molecular patterns (DAMPs) in the absence of pathogen-associated molecules. Macrophages, which are primarily localized in the tissue, play a pivotal role in sensing DAMPs. Furthermore, macrophages can also detect and respond to resolution-associated molecular patterns (RAMPs) and specific pro-resolving mediators (SPMs) during sterile inflammation. Macrophages, being highly adaptable cells, are particularly influenced by changes in the microenvironment. In response to the tissue environment, monocytes, pro-inflammatory macrophages, and pro-resolution macrophages can modulate their differentiation state. Ultimately, DAMP and RAMP-primed macrophages, depending on the predominant subpopulation, regulate the balance between inflammatory and resolving processes. While sterile injury and pathogen-induced reactions may have distinct effects on macrophages, most studies have focused on macrophage responses induced by pathogens. In this review, which emphasizes available human data, we illustrate how macrophages sense these mediators by examining the expression of receptors for DAMPs, RAMPs, and SPMs. We also delve into the signaling pathways induced by DAMPs, RAMPs, and SPMs, which primarily contribute to the regulation of macrophage differentiation from a pro-inflammatory to a pro-resolution phenotype. Understanding the regulatory mechanisms behind the transition between macrophage subtypes can offer insights into manipulating the transition from inflammation to resolution in sterile inflammatory diseases.

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Section: Comparison Of Ramp- and Damp-induced Signaling Pathways On P...mentioning

confidence: 99%

Damage-mediated macrophage polarization in sterile inflammation

et al. 2023

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“…Vascular diseases are mainly related to vascular lesions affecting the circulatory system, which affect the patients’ quality of life and seriously threaten their life and health [ 21 ]. Among these, cardiovascular diseases and cancer rank first and second, respectively, in terms of global mortality.…”

Section: Introductionmentioning

confidence: 99%

Insight into extracellular vesicles in vascular diseases: intercellular communication role and clinical application potential

Liu,

Jin,

Chen

et al. 2023

Cell Commun Signal

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Background Cells have been increasingly known to release extracellular vesicles (EVs) to the extracellular environment under physiological and pathological conditions. A plethora of studies have revealed that EVs contain cell-derived biomolecules and are found in circulation, thereby implicating them in molecular trafficking between cells. Furthermore, EVs have an effect on physiological function and disease development and serve as disease biomarkers. Main body Given the close association between EV circulation and vascular disease, this review aims to provide a brief introduction to EVs, with a specific focus on the EV cargoes participating in pathological mechanisms, diagnosis, engineering, and clinical potential, to highlight the emerging evidence suggesting promising targets in vascular diseases. Despite the expansion of research in this field, some noticeable limitations remain for clinical translational research. Conclusion This review makes a novel contribution to a summary of recent advances and a perspective on the future of EVs in vascular diseases.

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