Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Targeting TGFβ Signaling to Address Fibrosis Using Antisense Oligonucleotides

25 Jun 2018

Abstract excerpt

Fibrosis results from the excessive accumulation of extracellular matrix in chronically injured tissue. The fibrotic process is governed by crosstalk between many signaling pathways. The search for an effective treatment is further complicated by the fact that there is a degree of tissue-specificity in the pathways involved, although the process is not completely understood for all tissues. A plethora of drugs...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Muscle Physiology and Disorders
Share to Neurogenetic and Muscular Disorders Research
Share to RNA Interference and Gene Delivery

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 29941814
DOI: 10.3390/biomedicines6030074

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Targeting TGFβ Signaling to Address Fibrosis Using Antisense OligonucleotidesPMID 29941814Read ↗

Targeting TGF-β signaling for the treatment of fibrosisSemantic proximity Read ↗

Antisense Oligonucleotide-Based Therapy for Neuromuscular DiseaseSemantic proximity Read ↗

Targeting Fibrosis in Duchenne Muscular DystrophySemantic proximity Read ↗

Antisense oligonucleotide therapeutics targeting age-related diseasesSemantic proximity Read ↗

Antisense oligonucleotide-mediated exon skipping for Duchenne muscular dystrophy: progress and challenges.Semantic proximity Read ↗

Antisense oligonucleotides and other genetic therapies made simpleSemantic proximity Read ↗

Therapeutic pro-fibrogenic signaling pathways in fibroblastsSemantic proximity Read ↗

Splicing modulation therapy in the treatment of genetic diseasesSemantic proximity Read ↗

Translational development of splice-modifying antisense oligomersSemantic proximity Read ↗

Periostin exon 17 skipping enhances the efficacy of local AAV-microdystrophin administration in a fibrotic model of Duchenne muscular dystrophySemantic proximity Read ↗

Challenges to oligonucleotides-based therapeutics for Duchenne muscular dystrophySemantic proximity Read ↗

Modifying muscular dystrophy through transforming growth factor‐βSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.