Review
Cardiac & Cardiovascular Systems
Somayeh Saadat, Mahdi Noureddini, Maryam Mahjoubin-Tehran, Sina Nazemi, Layla Shojaie, Michael Aschner, Behnaz Maleki, Mohammad Abbasi-kolli, Hasan Rajabi Moghadam, Behrang Alani, Hamed Mirzaei
Summary: TGF-β induces cardiac fibrosis through activation of cytokines and growth factors, stimulating fibroblast proliferation and ECM protein production via canonical and non-canonical signaling pathways. Non-coding RNAs play crucial roles in regulating these processes, suggesting potential for new diagnostic and therapeutic approaches for cardiac disorders.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2021)
Article
Pharmacology & Pharmacy
Jin-xing Zhu, Wang Ling, Chao Xue, Zhen Zhou, Yi-shuai Zhang, Chen Yan, Mei-ping Wu
Summary: The study aimed to investigate the impact of Higenamine (HG) on chronic cardiac remodeling, particularly cardiac fibrosis. The results showed that HG could alleviate chronic cardiac hypertrophy, fibrosis, and dysfunction by suppressing TGF-β1/Smad signaling and the activation of cardiac fibroblasts (CFs).
EUROPEAN JOURNAL OF PHARMACOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Umadevi Subramanian, Chandramohan Ramasamy, Samivel Ramachandran, Joshua M. Oakes, Jason D. Gardner, Kailash N. Pandey
Summary: This study found that the development of cardiac fibrosis and dysfunction in Npr1 mutant mice is predominantly regulated through the TGF-beta 1-mediated SMAD-dependent pathway.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Biochemistry & Molecular Biology
Li-Li Ren, Xiao-Jun Li, Ting-Ting Duan, Zheng-Hai Li, Jun-Zheng Yang, Ya-Mei Zhang, Liang Zou, Hua Miao, Ying-Yong Zhao
Summary: Fibrosis is the excessive deposition of extracellular matrix components in the processes of tissue repair, causing organ structural integrity and functional impairment. Transforming growth factor-beta (TGF-beta) is a key factor in promoting fibrosis by activating profibrotic signals. This review discusses the role of TGF-beta signaling in fibrotic organs, as well as potential therapeutic options for targeting tissue fibrosis through modulating TGF-beta signaling.
CHEMICO-BIOLOGICAL INTERACTIONS
(2023)
Article
Plant Sciences
Junjun Li, Fuxing Ge, Shana Wuken, Shungang Jiao, Panlong Chen, Meiwen Huang, Xiaoli Gao, Juan Liu, Pengfei Tu, Xingyun Chai, Luqi Huang
Summary: This study aimed to investigate the cardioprotective properties and pharmacological mechanism of ZER against cardiac fibrosis. Animal experiments and in vitro studies showed that ZER can attenuate cardiac fibrosis and improve cardiac function by inhibiting the TGF-01/Smad signaling pathway.
Review
Cell Biology
Wuming Qin, Linghui Cao, Isaac Yaw Massey
Summary: Cardiac fibrosis is a common pathological change in heart failure and other cardiovascular diseases, with the PI3K/Akt signaling pathway playing a crucial role in regulating its occurrence, progression, and pathological formation.
MOLECULAR AND CELLULAR BIOCHEMISTRY
(2021)
Article
Agriculture, Multidisciplinary
Xuechun Sun, Yu Yang, Xiaodan Sun, Huali Meng, Wenhao Hao, Jialin Yin, Fuzhe Ma, Xin Guo, Lei Du, Lei Sun, Hao Wu
Summary: The current study investigated the preventive effect of krill oil (KO) on diabetic nephropathy (DN) and found that it can prevent DN by suppressing the TGF-beta 1 signaling pathway.
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
(2022)
Article
Cardiac & Cardiovascular Systems
Yifan Zhang, Bo Yuan, Yue Xu, Na Zhou, Ruiqi Zhang, Lan Lu, Zhanbin Feng
Summary: This study found that miR-208b and miR-21 promote the progression of cardiac fibrosis through activation of the TGF-beta 1/Smad-3 signaling pathway.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2022)
Review
Pharmacology & Pharmacy
Xiao-Yong Yu, Qian Sun, Ya-Mei Zhang, Liang Zou, Ying-Yong Zhao
Summary: This review summarizes the role of TGF-beta/Smad signaling pathway in tubulointerstitial fibrosis and natural products that target this pathway for the treatment of fibrosis. Additionally, it presents challenges and opportunities for inhibiting renal fibrosis in the future.
FRONTIERS IN PHARMACOLOGY
(2022)
Review
Biochemistry & Molecular Biology
Olga Kachanova, Arseniy Lobov, Anna Malashicheva
Summary: The Notch signaling pathway plays a cardioprotective role in heart development and recovery after myocardial infarction by reducing oxidative stress, preventing apoptosis, regulating inflammation, containing fibrosis and hypertrophy, promoting tissue revascularization, and regulating proliferation and differentiation of cardiomyocytes. It interacts with other signaling cascades involved in the pathogenesis and repair of myocardial infarction.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Integrative & Complementary Medicine
Kang Rong, Tian Wen, Cao Wei, Sun Yang, Zhang Hui-Nan, Feng Ying-Da, Li Chen, Li Ze-Zhi, Li Xiao-Qiang
Summary: LF delays liver fibrosis formation, decreases AST, ALT activities, and increases Alb activity in serum. It reduces oxidative damage, suppresses the TGF-beta/Smad signaling pathway, and plays a role in attenuating CCl4-induced liver fibrosis.
CHINESE JOURNAL OF NATURAL MEDICINES
(2021)
Article
Neurosciences
Vince Szegeczki, Helga Perenyi, Gabriella Horvath, Barbara Hinnah, Andrea Tamas, Zsolt Radak, Dora Abraham, Roza Zakany, Dora Reglodi, Tamas Juhasz
Summary: The study suggests that long-term training can reduce kidney fibrosis in AD mice, and TGF beta signaling plays a role in this phenomenon.
JOURNAL OF ALZHEIMERS DISEASE
(2021)
Article
Biochemistry & Molecular Biology
Dan Wang, Bochuan Deng, Lu Cheng, Jieru Li, Xiaomin Guo, Jiao Zhang, Xiang Zhang, Ping Su, Guofeng Li, Xiaokang Miao, Wenle Yang, Junqiu Xie, Rui Wang
Summary: In this study, a novel peptide DR4penA was designed based on the structure-activity relationship and rational design. DR4penA showed higher anti-PF activity, antioxidant activity, and a longer half-life compared to the original peptide DR8. It was found that DR4penA attenuated bleomycin- and paraquat-induced PF, and its anti-PF activity was equivalent to that of pirfenidone. Furthermore, DR4penA suppressed the TGF-beta/Smad pathway in TGF-beta 1-induced A549 cells and paraquat-induced rats. This study suggests that DR4penA is a potential candidate for PF therapy.
Article
Multidisciplinary Sciences
Meilinah Hidayat, Sijani Prahastuti, Ervi Afifah, Wahyu Widowati, Muhammad Yusuf, Khomaini Hasan
Summary: The study showed that PHGPB and LERGDT have anti-fibrotic effects on renal fibrosis by reducing TGF-beta 1 levels and SMAD gene expression, suggesting their potential as therapeutic options for improving renal function in fibrosis.
JOURNAL OF KING SAUD UNIVERSITY SCIENCE
(2022)
Article
Pharmacology & Pharmacy
Qian-rong Wang, Suo-si Liu, Jia-li Min, Min Yin, Yan Zhang, Yu Zhang, Xiang-ning Tang, Xia Li, Shan-shan Liu
Summary: Pulmonary fibrosis (PF) is a fatal respiratory disease with limited treatment options. The chemokine CCL17 plays a crucial role in the development of immune diseases, and its levels are elevated in PF patients. In this study, it was found that CCL17 is upregulated in the lungs of PF patients and mice with induced PF. The interaction between CCL17 and its receptor CCR4 activates the TGF-beta/Smad signaling pathway, promoting fibroblast activation and tissue fibrosis. Blocking CCL17 or CCR4 can inhibit fibroblast activation and tissue fibrosis, potentially benefiting patients with fibroproliferative lung diseases.
BIOCHEMICAL PHARMACOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Shuaibo Huang, Bijun Chen, Claudio Humeres, Linda Alex, Anis Hanna, Nikolaos G. Frangogiannis
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
(2020)
Review
Cardiac & Cardiovascular Systems
Anis Hanna, Nikolaos G. Frangogiannis
CARDIOVASCULAR DRUGS AND THERAPY
(2020)
Meeting Abstract
Cardiac & Cardiovascular Systems
Claudio D. Humeres, Arti V. Shinde, Anis Hanna, Simon Conway, Nikolaos G. Frangogiannis
Review
Cell Biology
Harikrishnan Venugopal, Anis Hanna, Claudio Humeres, Nikolaos G. Frangogiannis
Summary: This review discusses the mechanisms, roles, and fate of fibroblasts in the infarcted heart. Following a myocardial infarction, fibroblasts undergo phenotypic transitions and contribute to inflammatory, reparative, and angiogenic responses. They form collagen-based scars to protect the infarcted ventricle and may also stimulate angiogenesis. Prolonged activation of fibroblasts may contribute to adverse remodeling and heart failure.
Article
Biochemistry & Molecular Biology
Jun Li, Ruoshui Li, Izabela Tuleta, Silvia C. Hernandez, Claudio Humeres, Anis Hanna, Bijun Chen, Nikolaos G. Frangogiannis
Summary: The role of macrophage Smad7 in regulating inflammation and repair after myocardial infarction is limited. The anti-inflammatory effects of TGF-beta in macrophages are not restrained by endogenous Smad7 induction.
Article
Cardiac & Cardiovascular Systems
Bijun Chen, Ruoshui Li, Silvia C. Hernandez, Anis Hanna, Kai Su, Arti V. Shinde, Nikolaos G. Frangogiannis
Summary: TGF-beta signaling through Smad2/3 regulates macrophage responses in myocardial infarction. Smad3 plays a crucial role in mediating the anti-inflammatory and phagocytic effects of TGF-beta, while the activation of Smad2 does not affect these processes. Smad3, but not Smad2, is the main mediator of transcriptional effects of TGF-beta on macrophages.
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
(2022)
Article
Cardiac & Cardiovascular Systems
Linda Alex, Izabela Tuleta, Silvia C. Hernandez, Anis Hanna, Harikrishnan Venugopal, Maider Astorkia, Claudio Humeres, Akihiko Kubota, Kai Su, Deyou Zheng, Nikolaos G. Frangogiannis
Summary: This study found that pericytes in the heart play a role in tissue repair, remodeling, and fibrosis. After myocardial infarction, a subpopulation of pericytes exhibits transient expression of fibroblast markers and contributes to the formation of fibrotic tissue. Pericyte-specific TGF-beta signaling is involved in the maturation of blood vessels in the infarcted area and protects against adverse remodeling.
Article
Cardiac & Cardiovascular Systems
Linda Alex, Izabela Tuleta, Anis Hanna, Nikolaos G. Frangogiannis
Summary: Interstitial and perivascular fibrosis may contribute to diabetes-associated heart failure. Pericyte to fibroblast conversion is not the main mechanism of diabetic fibrosis, but a matrix-preserving fibroblast program is involved, which is independent of myofibroblast conversion and only partially explained by the hyperglycemic environment.
JOURNAL OF THE AMERICAN HEART ASSOCIATION
(2023)
Meeting Abstract
Cardiac & Cardiovascular Systems
Anis Hanna, Nikolaos Frangogiannis
Article
Medicine, Research & Experimental
Claudio Humeres, Arti V. Shinde, Anis Hanna, Linda Alex, Silvia C. Hernandez, Ruoshui Li, Bijun Chen, Simon J. Conway, Nikolaos G. Frangogiannis
Summary: Repair of the infarcted heart requires TGF-beta/Smad3 signaling in cardiac myofibroblasts, but it needs to be tightly regulated to prevent excessive fibrosis and adverse remodeling.
JOURNAL OF CLINICAL INVESTIGATION
(2022)
Meeting Abstract
Cardiac & Cardiovascular Systems
Anis Hanna, Nikolaos Frangogiannis
Meeting Abstract
Cardiac & Cardiovascular Systems
Claudio Humeres, Arti V. Shinde, Anis Hanna, Linda Alex, Simon Conway, Nikolaos G. Frangogiannis
CIRCULATION RESEARCH
(2021)
Meeting Abstract
Cardiac & Cardiovascular Systems
Ruoshui Li, Bijun Chen, Anis Hanna, Claudio Humeres, Linda Alex, Nikolaos G. Frangogiannis
CIRCULATION RESEARCH
(2021)
Article
Biochemistry & Molecular Biology
Anis Hanna, Arti V. Shinde, Ruoshui Li, Linda Alex, Claudio Humeres, Prasanth Balasubramanian, Nikolaos G. Frangogiannis
Summary: Tissue injury leads to alterations in collagen network, with specific patterns of collagen denaturation observed during different phases of infarct healing. MT1-MMP plays a significant role in pericellular collagen denaturation, while mechanical tension can induce peripheral collagen denaturation. Chronic collagen denaturation may contribute to post-infarction heart failure.
Article
Cell Biology
Ke Mi, Lizhong Zeng, Yang Chen, Jingya Ning, Siyuan Zhang, Peilin Zhao, Shuanying Yang
Summary: In this study, the researchers explored the role of DHX38 in NSCLC and its underlying molecular mechanism. They found that DHX38 was overexpressed in NSCLC and patients with high DHX38 expression had poor prognosis. DHX38 promoted cell proliferation, migration, and invasion in NSCLC and activated the MAPK pathway. The researchers also identified G3BP1 as a target protein that interacted with DHX38 and showed that DHX38 regulated the expression of G3BP1. Silencing G3BP1 reversed the effects of DHX38 overexpression on tumor cell proliferation, migration, and invasion and inhibited the MAPK pathway activation.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Tiina A. Jokela, Mark A. Dane, Rebecca L. Smith, Kaylyn L. Devlin, Sundus Shalabi, Jennifer C. Lopez, Masaru Miyano, Martha R. Stampfer, James E. Korkola, Joe W. Gray, Laura M. Heiser, Mark A. Labarge
Summary: Microenvironment signals have a significant impact on cell fate and tissue homeostasis. Understanding how different microenvironment factors regulate cellular phenotype has been challenging. In this study, a high-throughput microenvironment microarray was used to identify factors that support the proliferation and maintenance of primary human mammary luminal epithelial cells. Multiple factors that modulate luminal cell number were identified and their effects were confirmed using RNA sequencing and cell-based functional studies. Hepatocyte growth factor (HGF) was found to be robust to individual variation and played a role in expanding luminal cells. Our approach demonstrates the power of high-dimensional cell-based approaches in dissecting microenvironmental signals.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Chao He, Yongfeng Ding, Yan Yang, Gang Che, Fei Teng, Haohao Wang, Jing Zhang, Donghui Zhou, Yanyan Chen, Zhan Zhou, Haiyong Wang, Lisong Teng
Summary: This study categorized gastric cancer patients into three stemness subtypes, each demonstrating distinct prognoses, components of tumor microenvironment (TME) infiltration, and varying sensitivity or resistance to treatment. A stemness risk model was constructed to predict treatment response and prognosis.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Haile Zhao, Lijuan Feng, Rui Cheng, Man Wu, Xiaozhou Bai, Lifei Fan, Yaping Liu
Summary: miR-29c-3p is overexpressed in benign and malignant ovarian carcinoma and is associated with poor prognosis. Its overexpression modulates tumorigenesis in ovarian cancer cells, including epithelial-mesenchymal transition, proliferation, migration, and invasion, through the regulation of DNMT3A, TET1, and HBP1. miR-29c-3p may serve as a potential biomarker for clinical diagnosis or co-diagnosis of ovarian carcinoma.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Haiyan Zhao, Fangfang Bi, Mengyuan Li, Yuhan Diao, Chen Zhang
Summary: This study confirmed the tumor suppressor effect of RNF180 on ovarian cancer, elucidated the mechanism of the molecule network related to RNF180 and IPO4 in ovarian cancer, and identified a new therapeutic target for ovarian cancer.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Chu Chen, Guanhua Xu, Jiajia Chen, Chunshuai Wu, Jinlong Zhang, Jiawei Jiang, Hongxiang Hong, Zhiming Cui
Summary: This study investigated the role of transcription factor FoxO1 in facet joint osteoarthritis (FJOA) and found that FoxO1 deletion led to severe osteoarthritic changes. Transcriptome sequencing and bioinformatics analysis identified differentially expressed genes (DEGs) and potential key contributors to FJOA. Additionally, over-expression of certain genes and inhibition of others were shown to counteract the impairments caused by FoxO1 deletion in chondrocyte migration and extracellular matrix synthesis. These findings help unravel the molecular mechanisms underlying FJOA and open up promising therapeutic avenues for its treatment.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Wen Deng, Ru Chen, Situ Xiong, Jianqiang Nie, Hailang Yang, Ming Jiang, Bing Hu, Xiaoqiang Liu, Bin Fu
Summary: This study demonstrates that circFSCN1 is upregulated in bladder cancer and associated with cancer-specific survival. CircFSCN1 promotes tumor progression and epithelial-mesenchymal transition in bladder cancer through enhancing MDM2-mediated silencing of p53 by sponging miR-145-5p.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Jun Wu, Weibin Hu, Wenhui Yang, Yihao Long, Kaizhao Chen, Fugui Li, Xiaodong Ma, Xun Li
Summary: Cholesterol biosynthesis and metabolism play critical roles in tumor development and microenvironmental conditions. Squalene Epoxidase (SQLE), the second rate-limiting enzyme in cholesterol synthesis, is found to be uniquely expressed in various cancers, and its expression level is closely associated with tumor mutation burden and microsatellite instability. SQLE expression is negatively correlated with immune cell infiltration. Inhibition of SQLE alters the immune response in the tumor microenvironment. Furthermore, protein metabolism and translation are identified as main binding factors with SQLE.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Zhihong Zhang, Mingyue Li, Yi Tai, Yue Xing, Hongxiang Zuo, Xuejun Jin, Juan Ma
Summary: ZNF70 plays an important role in colitis-associated colorectal cancer (CAC) by regulating macrophages IL-1 beta secretion to promote HCT116 proliferation. It may serve as a promising target for treating CAC.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Zenghong Wu, Gangping Li, Weijun Wang, Kun Zhang, Mengke Fan, Yu Jin, Rong Lin
Summary: This study comprehensively explored the role of immune checkpoints and tumor microenvironment in gastric cancer patients based on genomic data. It constructed an ICIs signature and ICI score to evaluate patient prognosis and heterogeneity.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Yantong Wan, Jieshu Zhou, Panpan Zhang, Xuemei Lin, Hao Li
Summary: This study found that Rac1 plays a role in astrocyte activation and attenuates chronic inflammatory pain by blocking the phosphorylation of NLRP3 inflammasome and NF-kappa B.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Zhen Wang, Diankun She, Lei Liu, Xianming Hua, Hao Zhu, Lingfeng Yu, Han Wang, Yan Zhu, Gentao Fan, Yicun Wang, Meng Xu, Guangxin Zhou
Summary: Circular RNAs (circRNAs) are non-coding RNAs that play a role in the regulation of various cancers, including osteosarcoma (OS). This study identified circSATB2 as a highly expressed circRNA in OS tissues and cell lines, and demonstrated its involvement in promoting OS proliferation and migration. Mechanistically, circSATB2 was found to regulate the progression of OS by sponging miR-661 and FUS to regulate ZNFX1 mRNA. These findings suggest that circSATB2 could serve as a prognostic marker and therapeutic target for osteosarcoma.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Kenichi Ogata, Masafumi Moriyama, Tatsuya Kawado, Hiroki Yoshioka, Aiko Yano, Mayu Matsumura-Kawashima, Seiji Nakamura, Shintaro Kawano
Summary: This study found that extracellular vesicles released by induced pluripotent stem cells can reduce inflammatory cell infiltration, increase saliva volume, and decrease the production of antibodies associated with Sjogren's syndrome in a mouse model. The let-7 family in these vesicles may suppress the expression of TLR4 and NF-kappa B, which leads to the inhibition of pro-inflammatory cytokine production through the MAPK pathway.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Mikayla R. Erdelsky, Sarah A. Groves, Charmi Shah, Samantha B. Delios, M. Bibiana Umana, Donald H. Maurice
Summary: Recent evidence suggests that cAMP signaling within the primary cilium plays a crucial role in promoting adipogenic differentiation of 3T3-L1 preadipocytes. In this study, the researchers identified the specific cAMP phosphodiesterases expressed by these cells and found that inhibition of PDE4 promotes FFAR4-mediated adipogenesis. This work could potentially lead to the discovery of more targeted therapeutic approaches for controlling adipogenesis and differentiation of other stem cells.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Chun-Hui Liu, Jun-Jie Zhang, Qian-Jin Zhang, Yang Dong, Zhen-Duo Shi, Si-Hao Hong, Hou-Guang He, Wei Wu, Cong-Hui Han, Lin Hao
Summary: Bladder cancer, the most common malignant tumor in the urinary system, is associated with significantly up-regulated expression of P3H4, which is regulated by METTL3 and plays a crucial role in the proliferation, metastasis, and EMT progression of bladder cancer. Targeting this METTL3-P3H4 pathway may serve as a potential therapeutic strategy for bladder cancer.
CELLULAR SIGNALLING
(2024)