Pulmonary fibrosis (PF) is a progressive, and life-threatening interstitial lung disease which causes scarring in the lung parenchyma and thereby affects architecture and functioning of lung. It is an irreversible damage to lung functioning which is related to epithelial cell injury, immense accumulation of immune cells and inflammatory cytokines, and irregular recruitment of extracellular matrix. The inflammatory cytokines trigger the differentiation of fibroblasts into activated fibroblasts, also known as myofibroblasts, which further increase the production and deposition of collagen at the injury sites in the lung. Despite the significant morbidity and mortality associated with PF, there is no available treatment that efficiently and effectively treats the disease by reversing their underlying pathologies. In recent years, many therapeutic regimens, for instance, rho kinase inhibitors, Smad signaling pathway inhibitors, p38, BCL-xL/ BCL-2 and JNK pathway inhibitors, have been found to be potent and effective in treating PF, in preclinical stages. However, due to non-selectivity and non-specificity, the therapeutic molecules also result in toxicity mediated severe side effects. Hence, this review demonstrates recent advances on PF pathology, mechanism and targets related to PF, development of various drug delivery systems based on small molecules, RNAs, oligonucleotides, peptides, antibodies, exosomes, and stem cells for the treatment of PF and the progress of various therapeutic treatments in clinical trials to advance PF treatment. 

Emerging Delivery Approaches for Targeted Pulmonary Fibrosis Treatment

Aging is the most prominent nonmodifiable risk factor for various human diseases including Idiopathic pulmonary fibrosis. Aging progressively alters extracellular matrix components and is associated with the accumulation of senescent cells that promote age-related tissue dysfunction. In this review, we will discuss the pathological impact of aging and senescence on lung fibrosis via senescence-associated secretary phenotype factors and potential therapeutic approaches to limit the progression of lung fibrosis. 

The aged extracellular matrix and the pro-fibrotic role of senescence -associated secretory phenotype (SASP).

Modification of Extracellular Vesicle Surfaces: An Approach for Targeted Drug Delivery

Acute upper respiratory tract infections are a major public health issue, with uncontrolled inflammation triggered by upper respiratory viruses being a significant cause of patient deterioration or death. This study focuses on the Janus kinase-signal transducer and activator of transcription Rho-associated coiled-coil containing protein kinase (JAK-STAT-ROCK) signaling pathway, providing an in-depth analysis of the interplay between uncontrolled inflammation after upper respiratory tract infections and the development of neurodegenerative diseases. It offers a conceptual framework for understanding the lung-brain-related immune responses and potential interactions. The relationship between the ROCK-JAK-STAT signaling pathway and inflammatory immunity is a complex and multi-layered research area and exploring potential common targets could open new avenues for the prevention and treatment of related inflammation.

Novel Insights into the ROCK-JAK-STAT Signaling Pathway in Upper Respiratory Tract Infections and Neurodegenerative Diseases

Autotaxin Inhibition Reduces Post‐Ischemic Myocardial Inflammation via Epigenetic Gene Modifications

Pulmonary fibrosis is characterized by the accumulation of myofibroblasts in the lung and progressive tissue scarring. Fibroblasts exist across a spectrum of states, from quiescence in health to activated myofibroblasts in the setting of injury. Highly activated myofibroblasts have a critical role in the establishment of fibrosis as the predominant source of type 1 collagen and pro-fibrotic mediators. Myofibroblasts are also highly contractile cells and can alter lung biomechanical properties through tissue contraction. . One of the ways myofibroblast activation occurs is through activation of the Rho/myocardin-related transcription factor (MRTF) / serum response factor (SRF) pathway, which signals through intracellular actin polymerization. However, concerns surrounding the pleiotropic and ubiquitous nature of these signaling pathways have limited the translation of inhibitory drugs. Herein, we demonstrate a novel therapeutic anti-fibrotic strategy utilizing myofibroblast-targeted nanoparticles containing a MTRF/SRF pathway inhibitor (CCG-1423) which has been shown to block myofibroblast activation in vitro. Myofibroblasts were preferentially targeted via the angiotensin 2 receptor, which has been shown to be selectively upregulated in animal and human studies. These nanoparticles were non-toxic and accumulated in lung myofibroblasts in the bleomycin-induced mouse model of pulmonary fibrosis, reducing the number of these activated cells and their production of pro-fibrotic mediators. Ultimately, in a murine model of lung fibrosis, a single injection of these drug containing targeted nanoagents reduced fibrosis as compared to control mice. This approach has the potential to deliver personalized therapy by precisely targeting signaling pathways in a cell-specific manner, allowing increased efficacy with reduced deleterious off-target effects.

Myofibroblast-Specific Inhibition of the Rho Kinase-MRTF-SRF Pathway Using Nanotechnology for the Prevention of Pulmonary Fibrosis.

Extracellular Vesicles — A Versatile Biomaterial In article number 2101387 Rajendran J. C. Bose and co-workers demonstrate an effective anticancer therapy by developing PLGA-nanocarriers loaded with antimiRNA-21 or antimiRNA-10b using engineered tumor cell derived extracellular vesicles (eEVs) that display tumor specific receptor targeting peptide to achieve therapeutic effect by reprogramming cancer cells. 

Engineered Cell‐Derived Vesicles Displaying Targeting Peptide and Functionalized with Nanocarriers for Therapeutic microRNA Delivery to Triple‐Negative Breast Cancer in Mice (Adv. Healthcare Mater. 5/2022)

The spleen is an important mediator of both adaptive and innate immunity. As such, attempts to modulate the immune response provided by the spleen may be conducive to improved outcomes for numerous diseases throughout the body. Here, we use biomimicry to rationally design nanomaterials capable of splenic retention and immunomodulation for the treatment of disease in a distant organ, the post-infarct heart. Engineered senescent erythrocyte-derived nanotheranostic (eSENTs) were generated, demonstrating significant uptake by the immune cells of the spleen including T and B cells, as well as monocytes and macrophages. When loaded with suberoylanilide hydroxamic acid (SAHA), the nanoagents exhibit a potent therapeutic effect, reducing infarct size by 14% at 72 hours post-myocardial infarction when given as a single intravenous dose 2 hours after injury. These results are supportive of our hypothesis that RBC-derived biomimicry may provide new approaches for the targeted modulation of the pathological processes involved in myocardial infarction, thus further experiments to decisively confirm the mechanisms of action are currently underway. This novel concept may have far-reaching applicability for the treatment of a number of both acute and chronic conditions where the immune responses are either stimulated or suppressed by the splenic (auto)immune milieu. This article is protected by copyright. All rights reserved.

Biomimetic Nanomaterials for The Immunomodulation of The Cardiosplenic Axis Post-Myocardial Infarction.

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Myofibroblast-Specific Inhibition of the Rho Kinase-MRTF-SRF Pathway Using Nanotechnology for the Prevention of Pulmonary Fibrosis.

Engineered Cell‐Derived Vesicles Displaying Targeting Peptide and Functionalized with Nanocarriers for Therapeutic microRNA Delivery to Triple‐Negative Breast Cancer in Mice (Adv. Healthcare Mater. 5/2022)

Biomimetic Nanomaterials for The Immunomodulation of The Cardiosplenic Axis Post-Myocardial Infarction.