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Condition: Heart Failure
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Total 253 results found since Jan 2013.
Chaperone Mediated Autophagy Protects Cardiomyocytes Against Hypoxic-Cell Death
This study for the first time establishes a protective role for CMA (via Lamp2a overexpression) against hypoxia-induced cardiomyocyte loss and reveals the intriguing possibility that CMA activation may offer a cardioprotective treatment for ischemic heart disease.PMID:35584327 | DOI:10.1152/ajpcell.00369.2021
Source: Am J Physiol Cell Ph... - May 18, 2022 Category: Cytology Authors: Rajeshwary Ghosh Jennifer Jason Gillaspie Kenneth S Campbell J David Symons Sihem Boudina James Scott Pattison Source Type: research
The enigmatic role of VCAM-1 expressed by macrophages in mitochondrial metabolism and atherosclerosis
CONCLUSION: We conclude that macrophage-specific VCAM-1 augments mitochondrial biogenesis and DNA oxidation via Cmpk2. Oxidized mitochondrial DNA in plaque macrophages increases inflammation via Sting, resulting in exacerbation of atherosclerosis.PMID:35557156 | DOI:10.1096/fasebj.2022.36.S1.R6141
Source: Atherosclerosis - May 13, 2022 Category: Cardiology Authors: Niranjana Natarajan Jonathan Florentin Scott P O'Neil Lee L Ohayon Partha Dutta Source Type: research
CXCL10 is a novel anti ‐angiogenic factor downstream of p53 in cardiomyocytes
The conditioned media from p53-expressing cardiomyocytes decreased the tube formation of Rat Aortic Endothelial Cells. The blockade of CXCR3, a receptor of CXCL10, restored the angiogenic activity of the conditioned media from p53-expressing cardiomyocytes. AbstractTumor suppressor protein p53 plays crucial roles in the onset of heart failure. p53 activation results in cardiac dysfunction, at least partially by suppressing angiogenesis. Though p53 has been reported to reduce VEGF production by inhibiting hypoxia-inducible factor, the anti-angiogenic property of p53 remains to be fully elucidated in cardiomyocytes. To ex...
Source: Physiological Reports - May 11, 2022 Category: Physiology Authors: Tri Wahyuni,
Shota Tanaka,
Ryuta Igarashi,
Yoshiaki Miyake,
Ayaha Yamamoto,
Shota Mori,
Yusuke Kametani,
Masashi Tomimatsu,
Shota Suzuki,
Kosei Yokota,
Yoshiaki Okada,
Makiko Maeda,
Masanori Obana,
Yasushi Fujio Tags: ORIGINAL ARTICLE Source Type: research
Upregulation of Periostin Through CREB Participates in Myocardial Infarction-induced Myocardial Fibrosis
This study aims to verify the hypothesis that CREB promotes the expression of periostin in MI-induced myocardial fibrosis. To test this hypothesis, primary rat cardiac fibroblasts were cultured and rat model of MI was established. The level of myocardial fibrosis post-MI was identified by histological staining. The expressions of CREB and periostin were detected through western blot and reverse transcription quantity polymerase chain reaction. The upregulation and downregulation of CREB and periostin were established by plasmid, small interfere RNA (siRNA), and lentivirus, respectively. High levels of CREB and periostin we...
Source: Journal of Cardiovascular Pharmacology - May 1, 2022 Category: Cardiology Tags: Original Article Source Type: research
Dapagliflozin protects against doxorubicin-induced cardiotoxicity by restoring STAT3
Arch Toxicol. 2022 Apr 19. doi: 10.1007/s00204-022-03298-y. Online ahead of print.ABSTRACTDoxorubicin (Dox), an effective therapy in different types of cancer, is known to exhibit cardiotoxic effects. Despite previous studies indicating the benefits of dapagliflozin (DAPA) in patients experiencing heart failure, it remains uncertain whether DAPA exerts a protective effect on Dox-induced cardiac dysfunction. Signal transducer and activator of transcription 3 (STAT3) participates in various mechanisms of cardioprotection. Herein, we aimed to investigate the effects of DAPA on Dox-induced cardiotoxicity and the role of STAT3....
Source: Archives of Toxicology - April 19, 2022 Category: Toxicology Authors: Wei-Ting Chang Jhih-Yuan Shih Yu-Wen Lin Zhih-Cherng Chen Wei-Chih Kan Tsung-Hsien Lin Chon-Seng Hong Source Type: research
Periplocymarin alleviates pathological cardiac hypertrophy via inhibiting the JAK2/STAT3 signalling pathway
J Cell Mol Med. 2022 Apr 1. doi: 10.1111/jcmm.17267. Online ahead of print.ABSTRACTPathological cardiac hypertrophy is the most important risk factor for developing chronic heart failure. Therefore, the discovery of novel agents for treating pathological cardiac hypertrophy remains urgent. In the present study, we examined the therapeutic effect and mechanism of periplocymarin (PM)-mediated protection against pathological cardiac hypertrophy using angiotensinII (AngII)-stimulated cardiac hypertrophy in H9c2 cells and transverse aortic constriction (TAC)-induced cardiac hypertrophy in mice. In vitro, PM treatment significan...
Source: Molecular Medicine - April 2, 2022 Category: Molecular Biology Authors: Cai-Lian Fan Sui Liang Meng-Nan Ye Wan-Jun Cai Miao Chen Yun-Long Hou Jun Guo Yi Dai Source Type: research
