Role of genotoxic stressors and survival / metabolic pathways in inflammatory activation and cell recruitment in cardiovascular diseases, volume II

This Research Topic is the second volume of the series on the "Role of genotoxic stressors and survival / metabolic pathways in inflammatory activation and cell recruitment in cardiovascular diseases". Please see the first volume of this collection here.Genotoxic stressors (including those leading to DNA damage), survival/metabolic pathways (including autophagy and efferocytosis), and inflammatory activation are closely intertwined processes that significantly contribute to cardiovascular diseases (CVDs). DNA damage can occur due to factors like oxidative stress or environmental toxins, leading to genomic instability. The cell's DNA damage response (DDR) attempts to repair the damage, but when these mechanisms fail, chronic inflammation can be triggered, which is a hallmark of CVD progression.Autophagy and efferocytosis, as examples of pathway involved in the survival and metabolic response to genotoxic stressors, plays a vital role in maintaining cellular homeostasis by degrading damaged components, including misfolded proteins, organelles, and lipids. Importantly, autophagy facilitates the removal of cytosolic DNA, which, if left unchecked, can activate inflammatory pathways. In the context of CVDs, such as atherosclerosis and heart failure, impaired autophagy and defective efferocytosis leads to an accumulation of damaged DNA and proteins, thus exacerbating inflammation and disease progression.In addition to its role in mitigating inflammation, autophagy directly influences the cell’s ability to repair DNA damage. For example, autophagy provides resources necessary for the DNA repair process, including energy and precursors for nucleotide synthesis, and the regulation of the cGAS-STING pathway. When autophagy is deficient, DNA damage accumulates, fueling further inflammatory activation through pathways like NF-κB.Despite this understanding, significant gaps remain in the mechanistic links between genotoxic stressors, survival pathways, and inflammation. In addition, it is still controversial the contribution of selective inflammatory sub-populations, as well as their mechanism of recruitment and differentiation according to a selective stressor. Current research suggests that targeting survival pathways may present new therapeutic avenues to prevent damage-induced inflammation and its associated cardiovascular outcomes. As an example, current approaches focus on non-conventional molecules, like non-coding RNAs dissociation therapies, as therapeutic strategies to treat inflammatory activation. However, more research is required to fully elucidate these pathways and how they interact in the context of different cardiovascular conditions.In this Research Topic, we welcome the submission of manuscripts that cover recent advances in the following areas:• Immune cell subset differentiation and tissue inflammation under genotoxic stressors• Metabolic pathways involved in inflammation in CVD• Survival mechanisms against inflammation in CVD• Genotoxic damage in inflammatory cells in CVD• Novel therapeutic interventions against genotoxic insults mediating the inflammatory activation contributing at CVD progression• Novel therapeutic interventions modulating non-coding RNAs against genotoxic insults mediating the inflammatory activation contributing at CVD progression Topic editors: Lucia Natarelli, Floriana Farina, Federica Fogacci Source: https://www.frontiersin.org/research-topics/83853/role-of-genotoxic-stressors-and-survival-metabolic-pathways-in-inflammatory-activation-and-cell-recruitment-in-cardiovascular-diseases-volume-ii