YAP/TAZ: Molecular pathway and disease therapy.

MedComm (2020)

State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology Sichuan University Chengdu Sichuan China.

Published: August 2023

The Yes-associated protein and its transcriptional coactivator with PDZ-binding motif (YAP/TAZ) are two homologous transcriptional coactivators that lie at the center of a key regulatory network of Hippo, Wnt, GPCR, estrogen, mechanical, and metabolism signaling. YAP/TAZ influences the expressions of downstream genes and proteins as well as enzyme activity in metabolic cycles, cell proliferation, inflammatory factor expression, and the transdifferentiation of fibroblasts into myofibroblasts. YAP/TAZ can also be regulated through epigenetic regulation and posttranslational modifications. Consequently, the regulatory function of these mechanisms implicates YAP/TAZ in the pathogenesis of metabolism-related diseases, atherosclerosis, fibrosis, and the delicate equilibrium between cancer progression and organ regeneration. As such, there arises a pressing need for thorough investigation of YAP/TAZ in clinical settings. In this paper, we aim to elucidate the signaling pathways that regulate YAP/TAZ and explore the mechanisms of YAP/TAZ-induce diseases and their potential therapeutic interventions. Furthermore, we summarize the current clinical studies investigating treatments targeting YAP/TAZ. We also address the limitations of existing research on YAP/TAZ and propose future directions for research. In conclusion, this review aims to provide fresh insights into the signaling mediated by YAP/TAZ and identify potential therapeutic targets to present innovative solutions to overcome the challenges associated with YAP/TAZ.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10412783PMC
http://dx.doi.org/10.1002/mco2.340DOI Listing

Publication Analysis

Top Keywords

yap/taz
11
potential therapeutic
8
yap/taz molecular
4
molecular pathway
4
pathway disease
4
disease therapy
4
therapy yes-associated
4
yes-associated protein
4
protein transcriptional
4
transcriptional coactivator
4

Similar Publications

Cigarette smoking is a well-known risk factor inducing the development and progression of various diseases. Nicotine (NIC) is the major constituent of cigarette smoke. However, knowledge of the mechanism underlying the NIC-regulated stem cell functions is limited.

View Article and Find Full Text PDF

Developmental dynamics mimicking inversely engineered pericellular matrix for articular cartilage regeneration.

Biomaterials

December 2024

School of Medicine, Nankai University, Tianjin, 300071, PR China; Institute of Orthopedics, The First Medical Center, Chinese PLA General Hospital, Beijing Key Lab of Regenerative Medicine in Orthopedics, Key Laboratory of Musculoskeletal Trauma & War Injuries PLA, No. 28 Fuxing Road, Haidian District, Beijing, 100853, PR China; National Clinical Research Center for Orthopedics, Sports Medicine & Rehabilitation, Beijing, 100853, PR China. Electronic address:

The mechanical mismatch of scaffold matrix-mesenchymal stem cells (MSCs) has been a longstanding issue in the clinical application of MSC-based therapy for articular cartilage (AC) regeneration. Existing tissue-engineered scaffolds underestimate the importance of the natural chondrocyte pericellular matrix (PCM). Here, we reveal the temporal and spatial characteristics of collagen distribution around the chondrocytes.

View Article and Find Full Text PDF

PSAT1 promotes the progression of colorectal cancer by regulating Hippo-YAP/TAZ-ID1 axis via AMOT.

Mol Cell Biochem

December 2024

Department of Pathology, Nanfang Hospital, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, Guangdong, China.

Colorectal cancer (CRC) ranks third for morbidity and second for mortality among all digestive malignant tumors worldwide, but its pathogenesis remains not entirely clear. Bioinformatic analyses were performed to find out important biomarkers for CRC. For validation, reverse transcription-quantitative PCR, western blotting, and immunohistochemistry were performed.

View Article and Find Full Text PDF

Objective: To explore the influence of SALL4 in cardiac fibroblasts on the progression of myocardial infarction.

Methods: Analysis of genes specifically expressed in myocardial infarction by bioinformatics methods; The impact of SALL4 on myocardial infarction was assessed using mouse ultrasound experiments and Masson staining; The effect of SALL4 on the expression levels of collagen-I and collagen-III in myocardial tissue was examined by immunohistochemical staining; The migration ability of cardiac fibroblasts was evaluated using a Transwell assay; The proliferative ability of cardiac fibroblasts was tested using a CCK-8 assay; The relative fluorescence intensity of α-SMA and CTGF in cardiac fibroblasts were checked through immunofluorescence staining experiment; The expression of SALL4, DOT1L, H3K79me2, P53, SHP2, YAP, nucleus-YAP, collagen-I, α-SMA, CTGF, and PAI-1 in myocardial tissues or cardiac fibroblasts was detected using western blot analysis.

Results: SALL4-specific high expression in myocardial infarction; SALL4 intensified the alterations in the heart structure of mice with myocardial infarction and worsened the fibrosis of myocardial infarction; SALL4 also promoted the expression of SALL4, DOT1L, H3K79me2, P53, SHP2, YAP, nucleus-YAP, collagen-I, collagen-III, α-SMA, CTGF, and PAI-1 in myocardial infarction tissues and cardiac fibroblasts; Subsequently, SALL4 could enhance the immunofluorescence intensity of α-SMA and CTGF; Moreover, SALL4 could promote the proliferation and migration of cardiac fibroblasts.

View Article and Find Full Text PDF

Increased blood amino acid levels (hyperaminoacidemia) stimulate pancreas expansion by unclear mechanisms. Here, by genetic and pharmacological disruption of glucagon receptor (GCGR) in mice and zebrafish, we found that the ensuing hyperaminoacidemia promotes pancreatic acinar cell proliferation and cell hypertrophy, which can be mitigated by a low protein diet in mice. In addition to mammalian target of rapamycin complex 1 (mTORC1) signaling, acinar cell proliferation required , the most highly expressed amino acid transporter gene in both species.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!