Cardiac fibroblast in development and wound healing

Deb, Arjun; Ubil, Eric

doi:10.1016/j.yjmcc.2014.02.017

Cited by 132 publications

(114 citation statements)

References 78 publications

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“…Cardiac fibrosis is a basic pathological characteristic of the post-infarct myocardium and plays a pivotal role in the development of other cardiovascular diseases such as heart failure and atrial fibrillation [1] . Although ASA was reported to affect CF proliferation and migration in some situations stimulators, its function in the circumstance of cardiac fibrosis is not clear.…”

Section: Discussionmentioning

confidence: 99%

“…Cardiac fibrosis is a common pathological feature of many heart diseases [1] . Fibrosis leads to reduced cardiac pumping capacity and abnormal heart rhythms through elevated myocardial stiffness and impaired cardiac function, and it eventually leads to heart failure [2] .…”

Section: Introductionmentioning

confidence: 99%

“…Fibrosis leads to reduced cardiac pumping capacity and abnormal heart rhythms through elevated myocardial stiffness and impaired cardiac function, and it eventually leads to heart failure [2] . Cardiac fibrosis has been acknowledged as an early warning sign of sudden death for patients with heart failure [1] . However, few reports of medications that alleviate cardiac fibrosis have been published.…”

Section: Introductionmentioning

confidence: 99%

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Aspirin alleviates cardiac fibrosis in mice by inhibiting autophagy

Liu

Sun

et al. 2017

Acta Pharmacol Sin

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Aspirin (ASA) is a cardioprotective drug with anti-cardiac fibrosis action in vivo. This study was aimed to clarify the anti-cardiac fibrosis action of ASA and the underlying mechanisms. Two heart injury models (injection of isoproterenol and ligation of the left anterior descending branch) were used in mice to induce cardiac fibrosis. The animals were treated with ASA (10 mg·kg -1 ·d -1, ig) for 21 and 14 d, respectively. ASA administration significantly improved cardiac function, and ameliorated heart damage and fibrosis in the mice. The mechanisms underlying ASA's anti-fibrotic effect were further analyzed in neonatal cardiac fibroblasts (CFs) exposed to hypoxia in vitro. ASA (0.5-5 mmol/L) dose-dependently inhibited the proliferation and Akt phosphorylation in the CFs. In addition, ASA significantly inhibited CF apoptosis, and decreased the levels of apoptosis markers (cleaved caspase 3 and Parp1), which might serve as a side effect of anti-fibrotic effect of ASA. Furthermore, ASA dose-dependently inhibited the autophagy in the CFs, as evidenced by the reduced levels of autophagy marker LC3-II. The autophagy inhibitor Pepstatin A (PepA) promoted the inhibitory effect of ASA on CF proliferation, whereas the autophagy inducer rapamycin rescued ASA-caused inhibition of CF proliferation, suggesting an autophagydependent anti-proliferative effect of ASA. Both p38 inhibitor SB203580 and ROS scavenger N-acetyl-cysteine (NAC) significantly decreased Akt phosphorylation in CFs in the basal and hypoxic situations, but they both significantly increased LC3-II levels in the CFs. Our results suggest that an autophagy-and p38/ROS-dependent pathway mediates the anti-cardiac fibrosis effect of ASA in CFs. As PepA and SB203580 did not affect ASA-caused inhibition of CF apoptosis, the drug combination will enhance ASA's therapeutic effects.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Aspirin alleviates cardiac fibrosis in mice by inhibiting autophagy

Liu

Sun

et al. 2017

Acta Pharmacol Sin

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“…1,2,11,13,18,22,23 There is also increasing evidence that signaling pathways downstream of TGF-β1 receptors --both canonical Smad-dependent and noncanonical Smad-independent --are involved in mediating the effects of TGF-β1, including its antiapoptotic effect. 9,21,[33][34][35][36][37][38][39][40] Our findings in NIH/3T3 fibroblasts indicate that inhibition of a single pathway only partially reverses the antiapoptotic effect of TGF-β1, suggesting that both Smad-dependent and Erk1/2 pathways complement each other in suppression of apoptosis.…”

Section: A B Cmentioning

confidence: 99%

“…17 It is important to understand mechanisms underlying excessive fibrosis and identify targets to prevent such complications to reduce morbidity and mortality associated with the growing epidemic of aging-associated diseases. 2,4,12,14,[18][19][20][21][22][23] Transforming growth factor-β1 (TGF-β1), a profibrotic cytokine, has a variable effect on cell survival and proliferation depending on the cell type and clinical condition, with both proapoptotic and antiapoptotic effects previously described. 24 The effect of TGF-β1 receptor activation on differentiation and maturation of fibroblasts is mediated through two intracellular signaling pathways: 1) canonical, Smad-dependent, and 2) noncanonical, Erk1/2-dependent.…”

mentioning

confidence: 99%

TGF-β1 Increases Resistance of NIH/3T3 Fibroblasts Toward Apoptosis Through Activation of Smad2/3 and Erk1/2 Pathways

Negmadjanov¹,

Holmuhamedov²,

Emelyanova³

et al. 2016

Journal of Patient-Centered Research and Reviews

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Journal of Patient-Centered Research and Reviews ( JPCRR) is a peerreviewed scientific journal whose mission is to communicate clinical and bench research findings, with the goal of improving the quality of human health, the care of the individual patient, and the care of populations. Recommended CitationNegmadjanov U, Holmuhamedov A, Emelyanova L, Xu H, Rizvi F, Ross GR, Tajik AJ, Shi Y, Holmuhamedov E, Jahangir A. TGF-β1 increases resistance of NIH/3T3 fibroblasts toward apoptosis through activation of Smad2/3 and Erk1/2 pathways. J Patient Cent Res Rev. 2016;3:187-98.

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Modeling the Human Scarred Heart In Vitro: Toward New Tissue Engineered Models

Deddens

Sadeghi

Hjortnaes

et al. 2016

Adv Healthcare Materials

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Cardiac remodeling is critical for effective tissue healing, however, excessive production and deposition of extracellular matrix components contribute to scarring and failing of the heart. Despite the fact that novel therapies have emerged, there are still no lifelong solutions for this problem. An urgent need exists to improve the understanding of adverse cardiac remodeling in order to develop new therapeutic interventions that will prevent, reverse, or regenerate the fibrotic changes in the failing heart. With recent advances in both disease biology and cardiac tissue engineering, the translation of fundamental laboratory research toward the treatment of chronic heart failure patients becomes a more realistic option. Here, the current understanding of cardiac fibrosis and the great potential of tissue engineering are presented. Approaches using hydrogel-based tissue engineered heart constructs are discussed to contemplate key challenges for modeling tissue engineered cardiac fibrosis and to provide a future outlook for preclinical and clinical applications.

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Cardiac fibroblast in development and wound healing

Cited by 132 publications

References 78 publications

Aspirin alleviates cardiac fibrosis in mice by inhibiting autophagy

Aspirin alleviates cardiac fibrosis in mice by inhibiting autophagy

TGF-β1 Increases Resistance of NIH/3T3 Fibroblasts Toward Apoptosis Through Activation of Smad2/3 and Erk1/2 Pathways

Modeling the Human Scarred Heart In Vitro: Toward New Tissue Engineered Models

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