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Fibroblast and Immune Cell Cross Talk in Cardiac Repair
Published in Shyam S. Bansal, Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Stelios Psarras, Georgina Xanthou
Thus, the modulation of the immune response is capable of beneficially altering the activation status of fibroblasts, the pillars of cardiac fibrosis. Remarkably, established cardiac fibrosis can be modified, as myofibroblasts even from end-stage HF patients can partially reverse their pathogenic phenotype upon treatment with TGFβ1 inhibitors (117). More recent advances allow the in vivo targeting of pathogenic fibroblasts using T cells engineered to attack fibrotic fibroblasts with chimeric antigen receptor (CAR-T) technology (118). Given the scarcity of human cardiac samples, ex vivo systems using three-dimensional approaches (119), as well as cardiac biopsy material obtained during left-ventricular assist device (LVAD) implantation (120), may provide invaluable tools to study intercellular communication in the diseased heart and reveal novel therapeutic targets.
Potential of Fenugreek in Management of Fibrotic Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Amit D. Kandhare, Sunil Bhaskaran, Subhash L. Bodhankar
Cardiovascular diseases, including cardiac fibrosis, are recognized as vital predisposition factors for cardiac failure (Hinderer and Schenke-Layland 2019; Mozaffarian et al. 2015). The abnormal and excessive ECM deposition (such as type I collagen) results in impaired myocardial tissue function during cardiac remodeling and fibrosis (Hinderer and Schenke-Layland 2019). Furthermore, type I and type III collagen and their ratio during the myocardial infarction and ischemic cardiomyopathy are essential factors for cardiac fibrosis (Hinderer and Schenke-Layland 2019).
Heart failure with preserved ejection fraction in older adults
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Bharathi Upadhya, Dalane W. Kitzman
Early studies in HFpEF suggested that concentric LVH with normal chamber size was typical (37,38). However, subsequent studies have shown that many HFpEF patients have concentric remodeling without hypertrophy or even normal LV geometry (39–41). A recent trial of well-characterized HFpEF patients showed only 8% of patients had LVH at baseline and 50% had significant or severe diastolic dysfunction at rest (42). Similarly Maurer and colleagues found no significantly increased LV mass in older HFpEF patients in a community population compared to age- and gender-matched controls with hypertension (HTN) but not HF (43,44). In addition, while cardiac fibrosis is commonly present in HFpEF, the degree of fibrosis appears relatively modest (45). Thus, contrary to prior assumptions, LVH may not be a unique or fundamental feature of HFpEF.
Specific FSTL1 polymorphism may determine the risk of cardiomyopathy in patients with acromegaly
Published in Acta Cardiologica, 2022
Suleyman Nahit Sendur, Tuncay Hazirolan, Busra Aydin, Incilay Lay, Mehmet Alikasifoglu, Tomris Erbas
Interstitial fibrosis is a constant finding in acromegalic cardiomyopathy. Late gadolinium enhancement is a technique to allows determination of regional myocardial fibrosis in CMRI [31]. In our study, LGE was present in 20 (45.4%) out of 46 acromegalic subjects. In an autopsy report of 27 acromegalic subjects, Lie et al found interstitial fibrosis in 85% of cases [10]. Moreover, using ultrasonic cardiac tissue characterisation, Bogazzi et al showed cardiac fibrosis with a 53.7% prevalence. However, in the two earlier studies that used cardiac MRI to assess cardiac fibrosis, the prevalence of cardiac fibrosis was found to be low, 0 and 13.5% [32,33]. Contrary to the previous reports that assess cardiac fibrosis with CMRI, regional interstitial fibrosis was more frequent in our cohort.
Dysregulation of lncRNA-H19 in cardiometabolic diseases and the molecular mechanism involved : a systematic review
Published in Expert Review of Molecular Diagnostics, 2021
Ana Iris Hernández-Aguilar, Carlos Aldair Luciano-Villa, Vianet Argelia Tello-Flores, Fredy Omar Beltrán-Anaya, Ma Isabel Zubillaga-Guerrero, Eugenia Flores-Alfaro
Renal fibrosis is characterized by excessive deposition of the extracellular matrix in the interstitial compartment, leading to scar formation. An activated form of interstitial fibroblasts (α-smooth muscle actin-positive myofibroblasts) is widely recognized as the major type of matrix-producing cells in the fibrotic kidney [72]. The activity of lncRNA H19 in the kidney associated with the signaling pathways is similar to that observed in cardiac fibrosis, mainly in inflammatory activity and fibrosis, is poorly understood. In renal fibrosis, similar to other organs, changes in cell morphology and proliferation occur due to the overactivation of the molecular pathways involved in these processes, which leads to a decrease in their functions. Interstitial fibroblasts and EndMT are known to be the best-described mechanisms in the development of fibrosis and progression to renal failure [73].
Long non coding RNA H19: An emerging therapeutic target in fibrosing diseases
Published in Autoimmunity, 2020
Juan Li, Long-Ting Cao, Hong-Hui Liu, Xiao-Dong Yin, Jing Wang
Cardiac fibrosis is characterised by net accumulation of ECM proteins in the cardiac interstitium and contributes to both systolic and diastolic dysfunction in many cardiac pathological conditions, including hypertension, coronary heart disease, and heart failure [46]. Cardiac fibrosis is closely related to multiple cardiovascular system diseases, and noncoding RNAs (ncRNAs), including lncRNA and miRNA, have been reported to play a vital role in fibrogenesis. Emerging evidence showed that H19 endogenous expression is overexpressed in cardiac fibroblast and fibrosis tissues, namely H19 contributes to cardiac fibroblast proliferation and fibrosis [19]. Additionally, previous study explained that H19 knockdown could enhance the antifibrotic role of miR-455 and attenuate the connective tissue growth factor (CTGF) expression and further decrease cardiac fibrosis-associated protein synthesis (collagen I, III and α-SMA (a contractile protein and marker of profibrogenic cardiac fibroblast activation)), suggesting H19 potential therapeutic role in cardiac diseases [47]. These studies have laid strong foundations for the future development of novel treatments for cardiac fibrosis.