The Pathogenesis of Cardiac Fibrosis: A Review of Recent Progress

Maruyama, Kazuaki; Imanaka‐Yoshida, Kyoko

doi:10.3390/ijms23052617

Cited by 92 publications

(70 citation statements)

References 240 publications

(274 reference statements)

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“…The lymphatic vascular system plays diverse roles in the maintenance of tissue fluid balance, immune surveillance, lipid absorption from the gut, and tumor metastasis ( Oliver and Alitalo, 2005 ). Furthermore, recent progress in molecular and cellular characterization has unveiled the processes involved in the development of the lymphatic vasculature and the roles played by the lymphatic vasculature in various pathophysiological conditions ( Klaourakis et al, 2021 ; Maruyama et al, 2021 ; Maruyama and Imanaka-Yoshida, 2022 ; Oliver et al, 2020 ; Oliver and Alitalo, 2005 ).…”

Section: Introductionmentioning

confidence: 99%

The cardiopharyngeal mesoderm contributes to lymphatic vessel development in mouse

Maruyama

Miyagawa‐Tomita

Haneda

et al. 2022

eLife

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Lymphatic vessels are crucial for tissue homeostasis and immune responses in vertebrates. Recent studies have demonstrated that lymphatic endothelial cells (LECs) arise from both venous sprouting (lymphangiogenesis) and de novo production from non-venous origins (lymphvasculogenesis), which is similar to blood vessel formation through angiogenesis and vasculogenesis. However, the contribution of LECs from non-venous origins to lymphatic networks is considered to be relatively small. Here, we identify the Islet1 (Isl1)-expressing cardiopharyngeal mesoderm (CPM) as a non-venous origin of craniofacial and cardiac LECs. Genetic lineage tracing with Isl1Cre/+ and Isl1CreERT2/+ mice suggested that a subset of CPM cells gives rise to LECs. These CPM-derived LECs are distinct from venous-derived LECs in terms of their developmental processes and anatomical locations. Later, they form the craniofacial and cardiac lymphatic vascular networks in collaboration with venous-derived LECs. Collectively, our results demonstrate that there are two major sources of LECs, the cardinal vein and the CPM. As the CPM is evolutionarily conserved, these findings may improve our understanding of the evolution of lymphatic vessel development across species. Most importantly, our findings may provide clues to the pathogenesis of lymphatic malformations, which most often develop in the craniofacial and mediastinal regions.

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Section: Introductionmentioning

confidence: 99%

The cardiopharyngeal mesoderm contributes to lymphatic vessel development in mouse

Maruyama

Miyagawa‐Tomita

Haneda

et al. 2022

eLife

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“…Cardiac fibrosis is a crucial pathological change of ventricular remodeling and a common consequence of multitudinous cardiovascular diseases, resulting in stiffer tissue and cardiac dysfunction. Therefore, effective antifibrotic therapies are essential to improving prognoses of these diseases [ 31 ]. Unfortunately, the current medicines have not been sufficiently successful in treating cardiac fibrosis.…”

Section: Discussionmentioning

confidence: 99%

miR-409-3p Regulated by GATA2 Promotes Cardiac Fibrosis through Targeting Gpd1

Wang

Yin

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Cardiac fibrosis is a hallmark of numerous chronic cardiovascular diseases that leads to heart failure. However, there is no validated therapy for it. Dysregulation of microRNAs has been confirmed to be involved in cardiac fibrosis development. However, the regulatory network was not well explored. This study was the first to highlight the role and molecular mechanism of miR-409-3p in cardiac fibrosis. We found that miR-409-3p was consistently increased in three fibrotic models, including heart tissues of postmyocardial infarction (MI) mice and neonatal rat cardiac fibroblasts treated with angiotensin II (Ang II) or transforming growth factor-β (TGF-β). Furthermore, myocardial infarction surgery-induced cardiac fibrosis and dysfunction were attenuated by systemic delivery of miR-409-3p antagomir. Notably, transfection with miR-409-3p mimics promoted the proliferation of cardiac fibroblasts and fibroblast-to-myofibroblast differentiation, accompanied by upregulated expression of Col1a1, Col3a1, and α-SMA. On the contrary, the miR-409-3p inhibitor exhibited the opposite effect. Following this, we verified Gpd1 as a direct target of miR-409-3p. Gpd1 siRNA abolished the antifibrotic effect of miR-409-3p inhibitor in neonatal rat cardiac fibroblasts, suggesting that miR-409-3p promotes cardiac fibrosis at least partially through Gpd1. Moreover, GATA2 was identified as a cardiac fibrosis-associated upstream positive transcription factor of miR-409-3p. Finally, these findings suggest that modulating miR-409-3p could be a potential therapeutic method for cardiac fibrosis.

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“…В последние годы изучается возможность потенцирования этого эффекта путем направленного воздействия на ключевые механизмы патологического накопления коллагена и изменения его композиции в интерстиции, а также ведется поиск возможных терапевтических мишеней (галектин-3, матриксные металлопротеиназы, тканевый ингибитор матриксных металлопротеиназ 1, фактор дифференцировки роста-15, остеопонтин и др.) [148][149][150][151][152][153][154][155][156][157] Коррекция провоспалительного статуса Существенное значение патологии иммунной системы в механизмах ХСН является хорошо доказанным фактом [158][159][160][161]. В качестве перспективных мишеней терапии, направленной на снижение выраженности провоспалительных сдвигов на системном и локальном уровне, а также готовности кардиомиоцитов к реализации программ апоптоза, пироптоза и аутофагии, чаще всего обозначают Toll-подобные рецепторы, инфламмасомы (включая NODподобные рецепторы), цитокины, а также апоптотические и пироптотические эффекторные механизмы [162][163][164][165][166][167][168][169][170][171][172][173].…”

Section: лечебные подходыunclassified

Promising directions in the treatment of chronic heart failure: improving old or developing new ones?

et al. 2022

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Unprecedented advances of recent decades in clinical pharmacology, cardiac surgery, arrhythmology, and cardiac pacing have significantly improved the prognosis in patients with chronic heart failure (CHF). However, unfortunately, heart failure continues to be associated with high mortality. The solution to this problem consists in simultaneous comprehensive use in clinical practice of all relevant capabilities of continuously improving methods of heart failure treatment proven to be effective in randomized controlled trials (especially when confirmed by the results of studies in real clinical practice), on the one hand, and in development and implementation of innovative approaches to CHF treatment, on the other hand. This is especially relevant for CHF patients with mildly reduced and preserved left ventricular ejection fraction, as poor evidence base for the possibility of improving the prognosis in such patients cannot justify inaction and leaving them without hope of a clinical improvement in their condition. The lecture consistently covers the general principles of CHF treatment and a set of measures aimed at inotropic stimulation and unloading (neurohormonal, volumetric, hemodynamic, and immune) of the heart and outlines some promising areas of disease-modifying therapy.

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The Pathogenesis of Cardiac Fibrosis: A Review of Recent Progress

Cited by 92 publications

References 240 publications

The cardiopharyngeal mesoderm contributes to lymphatic vessel development in mouse

The cardiopharyngeal mesoderm contributes to lymphatic vessel development in mouse

miR-409-3p Regulated by GATA2 Promotes Cardiac Fibrosis through Targeting Gpd1

Promising directions in the treatment of chronic heart failure: improving old or developing new ones?

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