Article
Biochemistry & Molecular Biology
S. Bolivar, J. A. Espitia-Corredor, F. Olivares-Silva, P. Valenzuela, C. Humeres, R. Anfossi, E. Castro, R. Vivar, A. Salas-Hernandez, V. Pardo-Jimenez, G. Diaz-Araya
Summary: Cardiac fibroblasts (CF) play a key role in maintaining the extracellular matrix balance in cardiac tissue, while IFN-beta exhibits anti-fibrotic effects on CF through STAT1 and STAT2, with STAT3 showing no involvement.
Article
Cell Biology
Stephanie L. K. Bowers, Qinghang Meng, Yasuhide Kuwabara, Jiuzhou Huo, Rachel Minerath, Allen J. York, Michelle A. Sargent, Vikram Prasad, Anthony J. Saviola, David Ceja Galindo, Kirk C. Hansen, Ronald J. Vagnozzi, Katherine E. Yutzey, Jeffery D. Molkentin
Summary: Defective type I collagen in the heart leads to cardiomyopathy with fibroblast expansion, activation, and fibrotic ECM deposition. However, acute inhibition of type I collagen production can have an anti-fibrotic and anti-hypertrophic effect.
Review
Biochemistry & Molecular Biology
Chun Chou, Michael T. Chin
Summary: Hypertrophic cardiomyopathy (HCM) is a common inherited cardiovascular disorder with complex pathogenesis involving factors beyond sarcomere mutations. Research challenges the monogenic origin of HCM and emphasizes the importance of re-evaluating disease mechanisms.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Biotechnology & Applied Microbiology
Zhenhuan Chen, Haiwen Zhou, Xiantao Huang, Shaoyun Wang, Xiaochao Ouyang, Yunxia Wang, Qianqiang Cao, Liu Yang, Yu Tao, Hengli Lai
Summary: Cardiovascular risk factors have attracted increasing attention due to population aging, and cardiac hypertrophy is the initial step leading to heart failure. This study found that pirfenidone may have potential pharmacological effects in treating cardiac hypertrophy in mice.
Review
Cardiac & Cardiovascular Systems
Akitoshi Hara, Michelle D. Tallquist
Summary: The intricate interplay between inflammatory and reparative responses in the context of heart injury is central to the pathogenesis of heart failure. Recent studies have focused on the interplay between fibroblasts and immune cells, bringing us closer to the identification of cell type-specific targets for intervention.
CURRENT CARDIOLOGY REPORTS
(2023)
Article
Cardiac & Cardiovascular Systems
Katharina Doerr, Michael Kammer, Roman Reindl-Schwaighofer, Matthias Lorenz, Thomas Prikoszovich, Rodrig Marculescu, Dietrich Beitzke, Alice Wielandner, Reinhold G. Erben, Rainer Oberbauer
Summary: The study aimed to investigate the effect of FGF23 suppression by calcimimetic therapy on LVH progression in patients with chronic kidney disease. The results showed that etelcalcetide treatment inhibited the progression of LVH compared to alfacalcidol, potentially reducing the risk of sudden cardiac death in this population.
CIRCULATION RESEARCH
(2021)
Article
Cardiac & Cardiovascular Systems
Natalie A. Noll, Lance A. Riley, Christy S. Moore, Lin Zhong, Mathew R. Bersi, James D. West, Roy Zent, W. David Merryman
Summary: This study found that the absence of Tln1 and Tln2 in cardiac fibroblasts leads to cardiomyocyte hypertrophy in response to ANG II in male mice, but results in a hypertrophy-resistant phenotype in female mice.
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Luping Wang, Panxia Wang, Suowen Xu, Zhuoming Li, Dayue Darrel Duan, Jiantao Ye, Jingyan Li, Yanqing Ding, Wenqing Zhang, Jing Lu, Peiqing Liu
Summary: This study investigates the crosstalk between C/EBP beta PARylation and SUMOylation during cardiac hypertrophy. The findings show that accumulation of PARylation on C/EBP beta at K134 site leads to downregulation of SUMOylation and contributes to cardiac hypertrophy. The study highlights the importance of the interaction between C/EBP beta PTMs, suggesting potential therapeutic strategies targeting PARP1 and activating C/EBP beta SUMOylation for treating cardiac hypertrophy.
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
(2022)
Article
Peripheral Vascular Disease
Matthew A. Sparks, Fitra Rianto, Edward Diaz, Ritika Revoori, Thien Hoang, Lucas Bouknight, Johannes Stegbauer, Anuradha Vivekanandan-Giri, Phillip Ruiz, Subramaniam Pennathur, Dennis M. Abraham, Susan B. Gurley, Steven D. Crowley, Thomas M. Coffman
Summary: Deletion of AT(1A) receptors in cardiomyocytes plays a crucial role in regression of cardiac hypertrophy, independent of reducing pressure overload.
Article
Cardiac & Cardiovascular Systems
Xiangxiang Wei, Jiayu Jin, Jian Wu, Yunquan He, Jieyu Guo, Zhaohua Yang, Liang Chen, Kui Hu, Liliang Li, Mengping Jia, Qinhan Li, Xiaoyu Lv, Fei Ge, Siyu Ma, Huijie Wu, Xiuling Zhi, Xinhong Wang, Lindi Jiang, Elena Osto, Jianyi Zhang, Dan Meng
Summary: This research investigates the function and mechanisms of BACH1 in the regulation of cardiac hypertrophy. The study found that cardiac-specific knockout of BACH1 protected against cardiac hypertrophy induced by Ang II or TAC, while cardiac-specific overexpression of BACH1 exaggerated cardiac hypertrophy and fibrosis. Mechanistically, BACH1 regulated the AT1R expression and the Ca2+/CaMKII pathway to mediate cardiac hypertrophy.
CARDIOVASCULAR RESEARCH
(2023)
Article
Cardiac & Cardiovascular Systems
Meryl Musicante, Hannah H. Kim, Yuanjian Chen, Fang Liao, Syamal K. Bhattacharya, Lu Lu, Yao Sun
Summary: This study revealed that eNOS plays a beneficial role in preventing cardiac myocyte hypertrophy and fibrosis, supporting the idea that eNOS may modify the severity of HCM phenotypes.
INTERNATIONAL JOURNAL OF CARDIOLOGY
(2022)
Article
Health Care Sciences & Services
Richard J. Roberts, Logan Hallee, Chi Keung Lam
Summary: Hsp90 is a key molecular chaperone that interacts with numerous disease pathways in cells, making it a potential therapeutic target. While small-molecule inhibition of Hsp90 activity may have cardiac toxicity, targeting Hsp90 through modulation of post-translational modifications (PTMs) could be a more attractive therapeutic strategy.
JOURNAL OF PERSONALIZED MEDICINE
(2021)
Review
Pathology
Ahmed Hjazi, Rasha Fadhel Obaid, Sally Saad Ali, Bekhzod Abdullaev, Hashem O. Alsaab, Huldani Huldani, Rosario Mireya Romero-Parra, Yasser Fakri Mustafa, Beneen M. Hussien, Sarah Jaafar Saadoon
Summary: Long non-coding RNAs (lncRNAs) transcribed from the human genome have emerged as important regulators in cellular activities, particularly in controlling gene expression. They have been found to regulate various factors related to tumorigenesis through the JAK-STAT signaling pathway, either by directly targeting or indirectly modulating its components. Moreover, lncRNAs can also act as downstream effectors of the pathway. The relationship between JAK-STAT signaling and lncRNAs varies among different types of cancers, and lncRNAs play a dual role in tumorigenesis or tumor suppression. This review focuses on the reciprocal regulation and functions of lncRNAs and the JAK-STAT pathway, providing insights into potential targets for clinical therapeutics.
PATHOLOGY RESEARCH AND PRACTICE
(2023)
Article
Pharmacology & Pharmacy
Bin Tu, Kai Song, Yang Zhou, He Sun, Zhi-Yan Liu, Li-Chan Lin, Ji-Fei Ding, Ji-Ming Sha, Yan Shi, Jing-Jing Yang, Rui Li, Ye Zhang, Jian-Yuan Zhao, Hui Tao
Summary: This study found that dysregulated mitochondrial fission plays a role in cardiac fibrosis, leading to proliferation and migration of cardiac fibroblasts. The researchers discovered that increased expression of METTL3 gene causes excessive mitochondrial fission, promoting fibroblast proliferation and migration, thus aggravating cardiac fibrosis. Inhibiting the expression of METTL3 gene can suppress mitochondrial fission, reduce fibroblast proliferation and migration, and improve cardiac fibrosis.
PHARMACOLOGICAL RESEARCH
(2023)
Article
Peripheral Vascular Disease
Alexandra M. Garvin, Matthew D. De Both, Joshua S. Talboom, Merry L. Lindsey, Matthew J. Huentelman, Taben M. Hale
Summary: Transient ACE inhibition in spontaneously hypertensive rats leads to a persistent shift in cardiac fibroblast subpopulations, resulting in reduced fibrogenic phenotype.
Article
Cell Biology
Ritwik Datta, Trisha Bansal, Santanu Rana, Kaberi Datta, Shiladitya Chattopadhyay, Mamta Chawla-Sarkar, Sagartirtha Sarkar
CELLULAR SIGNALLING
(2015)
Article
Chemistry, Multidisciplinary
Santanu Rana, Kaberi Datta, Teegala Lakshminarayan Reddy, Emeli Chatterjee, Preeta Sen, Manika Pal-Bhadra, Utpal Bhadra, Arindam Pramanik, Panchanan Pramanik, Mamta Chawla-Sarkar, Sagartirtha Sarkar
JOURNAL OF CONTROLLED RELEASE
(2015)
Article
Biochemistry & Molecular Biology
Arkadeep Mitra, Trayambak Basak, Shadab Ahmad, Kaberi Datta, Ritwik Datta, Shantanu Sengupta, Sagartirtha Sarkar
JOURNAL OF MOLECULAR BIOLOGY
(2015)
Article
Multidisciplinary Sciences
Priyadarshini Chakrabarti, Santanu Rana, Sreejata Bandopadhyay, Dattatraya G. Naik, Sagartirtha Sarkar, Parthiba Basu
SCIENTIFIC REPORTS
(2015)
Article
Pharmacology & Pharmacy
Aramita Ray, Santanu Rana, Durba Banerjee, Arkadeep Mitra, Ritwik Datta, Shaon Naskar, Sagartirtha Sarkar
TOXICOLOGY AND APPLIED PHARMACOLOGY
(2016)
Article
Biochemistry & Molecular Biology
Arkadeep Mitra, Ritwik Datta, Santanu Rana, Sagartirtha Sarkar
JOURNAL OF CELLULAR BIOCHEMISTRY
(2018)
Article
Biochemical Research Methods
Kaberi Datta, Trayambak Basak, Swati Varshney, Shantanu Sengupta, Sagartirtha Sarkar
JOURNAL OF PROTEOMICS
(2017)
Article
Biochemistry & Molecular Biology
Santanu Rana, Ritwik Datta, Ratul Datta Chaudhuri, Emeli Chatterjee, Mamta Chawla-Sarkar, Sagartirtha Sarkar
ANTIOXIDANTS & REDOX SIGNALING
(2019)
Article
Multidisciplinary Sciences
Urbi Mukhopadhyay, Shampa Chanda, Upayan Patra, Arpita Mukherjee, Santanu Rana, Anupam Mukherjee, Mamta Chawla-Sarkar
SCIENTIFIC REPORTS
(2019)
Article
Multidisciplinary Sciences
Anupam Mittai, Santanu Rana, Rajni Sharma, Akhilesh Kumar, Rishikesh Prasad, Satish K. Raut, Sagartirtha Sarkar, Uma Nahar Saikia, Ajay Bahl, Perundurai S. Dhandapany, Madhu Khullar
SCIENTIFIC REPORTS
(2019)
Article
Multidisciplinary Sciences
Kanika Singh, Ankit Gupta, Ashish Sarkar, Ishita Gupta, Santanu Rana, Sagartirtha Sarkar, Sameena Khan
SCIENTIFIC REPORTS
(2020)
Review
Biochemistry & Molecular Biology
Abhi Dutta, Moumita Das, Ankita Ghosh, Santanu Rana
Summary: Pathological cardiac damage during heart failure is associated with the release of cell death and damage associated molecular patterns (DAMPs), which leads to sterile inflammation and maladaptive cardiac tissue remodeling. Circulating or cytosolic DNA fragments, including cell free DNA (cfDNA), can interact with nucleic acid sensors in neighboring cells, triggering intra- and inter-cellular signaling cascades that upregulate inflammatory mediators and induce oxidative stress. This can result in interstitial fibrosis, cardiomyocyte contractile dysfunction, and cell death. This review focuses on the association of cfDNA with heart failure and explores its potential as a therapeutic target for improving cardiac function.