Editorial: Volume II: fibrotic tissue remodeling as a driver of disease pathogenesis

Volume II: fibrotic tissue remodeling as a driver of disease pathogenesis Organ failure occurs when the resident tissues are unable to meet their metabolic needs and fail to perform their designated function.Many pathophysiological conditions can cause organ failure.Among them, fibrosis is a major contributor as it significantly perturbs the elasticity of the cells and renders them inefficient (Lieber and Ward, 2013).Initially, the research regarding organ pathophysiology was more focused towards deciphering the pathways leading to the death of the participating cells.However, in the last two decades, research on fibrotic tissue remodelling gained significant attention as it started to unravel subtle changes within the organ microenvironment during disease progression, not just in end-stage organ failure.Fibrosis is a slowly developing phenomenon that eventually causes tissue degeneration, leading to devastating consequences in organs like heart, kidney, lung and liver (Conte, 2021).It occurs due to excessive accumulation of fibrous connective tissue in the extracellular matrix (ECM) area of injured tissues resulting in a fibrotic scar.The basic components of this fibrotic scar are-a mixture of fibrotic cells and collagens, chiefly types I and III.If this fibrotic tissue accumulation occurs beyond a threshold level, eventually organ malfunction occurs (Davidson et al., 2020).Several pro-fibrotic factors and cytokines have been proposed to be the major mediators of fibrosis in various tissues (Al-Hatt et al., 2022).With the rapid advancement of techniques like ECM proteomics, several novel molecules are also being reported as causal factors in this process (Naba, 2023).In this issue, the objective was to delineate minute nuances of renal and cardiac fibrosis and their potential therapeutic measures.In this issue, two reviews, two original research articles and one perspective article encompassed the different aspects of fibrosis.Wang et al. contributed with a comprehensive review on renal fibrosis.The review summarized how renal fibrosis is a common manifestation of any chronic kidney disease.Although this occurs as a self-repair process in response to kidney damage, it seriously affects the renal filtration function and has almost no specific treatments (Basile et al., 2012).Hence, exploring targeted therapeutic measures is the need of the hour.It has been reported by many researchers that Histone deacetylases (HDACs) are major causal players in promoting renal fibrosis through epigenetic modifications involving non-histone (Tong, 2002;Kumar and Brooks, 2023).