Delving into the Latest Updates on PNA-33 with Synapse

Overview

Basic Info

Drug Type

asPNA

Synonyms-

Target

miR-33a

Action

antagonists

Mechanism

miR-33a antagonists(microRNA 33a antagonists)

Therapeutic Areas

Respiratory DiseasesOther Diseases

Active Indication

Idiopathic Pulmonary Fibrosis

Inactive Indication-

Originator Organization

Yale University

Active Organization

Yale University

Inactive Organization-

License Organization-

Drug Highest PhasePreclinical

First Approval Date-

Regulation-

Structure/Sequence

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Author: Schupp, Jonas C ; Cosmos, Carlos ; Dela Cruz, Charles S ; McDonough, John E ; Ibarra, Gabriel ; Liu, Xinran ; Rosas, Ivan ; Prasse, Antje ; Ahangari, Farida ; Kim, Jooyoung ; Sharma, Lokesh ; Adams, Taylor S ; Kaminski, Naftali ; Rose, Kadi-Ann S ; Ryu, Changwan ; Pradeep, Sai Pallavi ; Price, Nathan L ; Omote, Norihito ; Malik, Shipra ; DeIuliis, Giuseppe ; Aurelien, Nachelle R ; Fernández-Hernando, Carlos ; Villalba Nunez, Julian A ; Chioccioli, Maurizio ; Bahal, Raman ; Bärnthaler, Thomas ; Ding, Shuizi

Idiopathic pulmonary fibrosis (IPF) is a progressive and ultimately fatal disease. Recent findings have shown a marked metabolic reprogramming associated with changes in mitochondrial homeostasis and autophagy during pulmonary fibrosis. The microRNA-33 (miR-33) family of microRNAs (miRNAs) encoded within the introns of sterol regulatory element binding protein (SREBP) genes are master regulators of sterol and fatty acid (FA) metabolism. miR-33 controls macrophage immunometabolic response and enhances mitochondrial biogenesis, FA oxidation, and cholesterol efflux. Here, we show that miR-33 levels are increased in bronchoalveolar lavage (BAL) cells isolated from patients with IPF compared with healthy controls. We demonstrate that specific genetic ablation of miR-33 in macrophages protects against bleomycin-induced pulmonary fibrosis. The absence of miR-33 in macrophages improves mitochondrial homeostasis and increases autophagy while decreasing inflammatory response after bleomycin injury. Notably, pharmacological inhibition of miR-33 in macrophages via administration of anti-miR-33 peptide nucleic acids (PNA-33) attenuates fibrosis in different in vivo and ex vivo mice and human models of pulmonary fibrosis. These studies elucidate a major role of miR-33 in macrophages in the regulation of pulmonary fibrosis and uncover a potentially novel therapeutic approach to treat this disease.

100 Deals associated with PNA-33

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