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Last update 08 May 2025

ACTA1

Last update 08 May 2025

Basic Info

Synonyms

ACTA, ACTA1, actin alpha 1, skeletal muscle

+ [4]

Introduction

Actins are highly conserved proteins that are involved in various types of cell motility and are ubiquitously expressed in all eukaryotic cells.

Drugs associated with ACTA1

WO2023186189

Patent Mining

Target

ACTA1

Mechanism-

Active Org.

Yangzhou University

Originator Org.

Yangzhou University

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ACTA1

100 Translational Medicine associated with ACTA1

0 Patents (Medical) associated with ACTA1

1,741

Literatures (Medical) associated with ACTA1

01 Jun 2025·Stem Cell Research

Generation of an induced pluripotent stem cell line (NCHi023-A) from a 41-year-old male with nemaline myopathy carrying autosomal dominant ACTA1 c.809-10C>A mutation

Article

Author: Ye, Shiqiao ; Yu, Yang ; Zhao, Ming-Tao ; Zhu, Jingting ; Rashnonejad, Afrooz ; Hanley, Meghan ; Flanigan, Kevin ; Lin, Hui

Nemaline myopathy is a rare genetic condition characterized by weakened muscles due to thread-like rods, called nemaline bodies, in muscle fibers. This condition varies in time of onset and severity. Although there is no cure, therapies and treatments are available to reduce symptoms. This iPSC line, NCHi023-A, was reprogrammed using Sendai virus from skin fibroblasts from a male patient with nemaline myopathy carrying a pathogenic heterozygous ACTA1 mutation. Characterization of this line was successful, with validation of cell identity, normal morphology and karyotype, positive expression of germ layer and pluripotency markers, and negative expression for mycoplasma and transgenes.

01 May 2025·American Journal of Physiology-Lung Cellular and Molecular Physiology

Succinate aggravates pulmonary fibrosis through the succinate/SUCNR1 axis

Article

Author: Mooslechner, Agnes Anna ; Heinemann, Akos ; Angiari, Stefano ; Platzer, Wolfgang ; Kwapiszewska, Grazyna ; Schweighofer, Hannah ; Rajesh, Rishi ; Pahernik, Svetlana ; Benazzo, Alberto ; Bärnthaler, Thomas ; Marsh, Leigh ; Atallah, Reham ; Aigner, Clemens ; Lanz, Ilse

This paper highlights the role of the succinate/SUCNR1 axis in pulmonary fibrosis. Receptor activation leads to profibrotic changes in IPF patient-derived fibroblasts. This finding could also be replicated in a mouse model of pulmonary fibrosis.

01 Apr 2025·The American Journal of Pathology

Piezo2 Is a Key Mechanoreceptor in Lung Fibrosis that Drives Myofibroblast Differentiation

Article

Author: Sime, Patricia J ; Thatcher, Thomas H ; Robila, Valentina ; Perelas, Apostolos ; Camus, Sarah V ; Freeberg, Margaret A T

Idiopathic pulmonary fibrosis (IPF) and other progressive fibrotic interstitial lung diseases have limited treatment options. Fibroblasts are key effector cells that sense matrix stiffness through conformation changes in mechanically sensitive receptors, leading to activation of downstream profibrotic pathways. Here, the role of Piezo2, a mechanosensitive ion channel, in human and mouse lung fibrosis, and its function in myofibroblast differentiation in primary human lung fibroblasts (HLFs) was investigated. Human samples from patients with IPF and mouse tissue from bleomycin-induced pulmonary fibrosis were assessed. Primary HLFs from nonfibrotic donors were grown on substrates of different stiffness to induce myofibroblast differentiation and treated with a Piezo2 inhibitor. Piezo2 expression was up-regulated in tissue from patients with IPF and in fibrotic mouse lung tissue. Additionally, analysis of published single-cell RNA-sequencing data showed that Piezo2 was expressed in the profibrotic collagen triple helix repeat containing 1 (Cthrc1)⁺ fibroblast subpopulation. Myofibroblast differentiation was increased in HLFs grown on substrates with fibrotic levels of stiffness compared with that seen in softer substrates. Piezo2 inhibition reduced stiffness-induced expression α-smooth muscle actin and fibronectin in HLFs. Piezo2 expression was elevated in fibrotic lung disease in both patients and rodents, and its presence was key in the differentiation of fibroblasts to the profibrotic myofibroblasts. Blocking Piezo2 may play a key role in fibrosis and, thus, be a novel therapeutic approach to treat pulmonary fibrosis.

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