Perspective: Pathological transdifferentiation—a novel therapeutic target for cardiovascular diseases and chronic inflammation DOI Creative Commons

William Y. Yang,

Melissa Mahgoub,

Fatma Saaoud

и другие.

Frontiers in Cardiovascular Medicine, Год журнала: 2024, Номер 11

Опубликована: Ноя. 26, 2024

Pathological transdifferentiation, where differentiated cells aberrantly transform into other cell types that exacerbate disease rather than promote healing, represents a novel and significant concept. This perspective discusses its role potential targeting in cardiovascular diseases chronic inflammation. Current therapies mainly focus on mitigating early inflammatory response through proinflammatory cytokines pathways targeting, including corticosteroids, TNF-α inhibitors, IL-1β monoclonal antibodies blockers, IL-6 nonsteroidal anti-inflammatory drugs (NSAIDs), along with modulating innate immune memory (trained immunity). However, these approaches often fail to address long-term tissue damage functional regeneration. For instance, fibroblasts can transdifferentiate myofibroblasts cardiac fibrosis, endothelial may undergo mesenchymal transition (EndMT) vascular remodeling, resulting fibrosis impaired function. Targeting pathological transdifferentiation promising therapeutic avenue by focusing key signaling drive aberrant cellular phenotypic transcriptomic transitions. approach seeks inhibit or modulate plasticity effective regeneration prevent fibrosis. Such strategies have the inflammation, death, damage, providing more comprehensive sustainable treatment solution. Future research should understanding mechanisms behind identifying relevant biomarkers master regulators, developing preclinical clinical trials. Integrating new existing treatments could enhance efficacy improve patient outcomes. Highlighting as target paradigms, leading better management recovery of tissues

Язык: Английский

Metabolic dysfunction and insulin sensitizers in acute and chronic disease DOI Creative Commons
Jerry R. Colca, Kyle S. McCommis

Expert Opinion on Investigational Drugs, Год журнала: 2025, Номер unknown, С. 1 - 10

Опубликована: Фев. 6, 2025

The concept of insulin resistance has been a major topic for more than 5 decades. While there are several treatments that may impact resistance, this pathology is uniquely addressed by mitochondrially directed thiazolidinedione (TZD) sensitizers. Understanding mechanism action and consideration 'insulin resistance' as consequence metabolic inflammation allows new paradigm approaching chronic diseases. We review evolving understanding the mitochondrial pyruvate carrier (MPC) TZD sensitizers discuss how reprogramming metabolism impacts pleotropic pharmacology in multiple tissues. Additional lines investigation proposed. A change can facilitate rethinking clinical trials, specifically beyond treatment frank type 2 diabetes. There should be broader evaluation combination with weight loss lifestyle approaches across diseases/syndromes associated resistance. Finally, 'connecting all dots' to unwind interconnectedness cell biology involved syndromes impacted dysfunction efficacy also uncover molecular targets. New studies discovery development novel pharmacologic agents.

Язык: Английский

Процитировано

0

Oxidative phosphorylation and breast cancer progression: insights into PGC-1α’s role in mitochondrial function DOI
Rihab Akasha,

Jerlyn Apatan Enrera,

S. Fatima

и другие.

Naunyn-Schmiedeberg s Archives of Pharmacology, Год журнала: 2025, Номер unknown

Опубликована: Март 17, 2025

Язык: Английский

Процитировано

0

Immune Checkpoints Are New Therapeutic Targets in Regulating Cardio-, and Cerebro-Vascular Diseases and CD4+Foxp3+ Regulatory T Cell Immunosuppression DOI Creative Commons
Ying Shao,

William Y. Yang,

Gayani Nanayakkara

и другие.

International Journal of Drug Discovery and Pharmacology, Год журнала: 2024, Номер unknown, С. 100022 - 100022

Опубликована: Ноя. 26, 2024

Although previous reviews explored the roles of selected immune checkpoints (ICPs) in cardiovascular diseases (CVD) and cerebrovascular from various perspectives, many related aspects have yet to be thoroughly reviewed analyzed. Our comprehensive review addresses this gap by discussing cellular functions ICPs, focusing on tissue-specific microenvironment-localized transcriptomic posttranslational regulation ICP expressions, as well their functional interactions with metabolic reprogramming. We also analyze how 14 pairs including CTLA-4/CD86-CD80, PD1-PDL-1, TIGIT-CD155, regulate CVD pathogenesis. Additionally, covers ICPs modulating CD4+Foxp3+ regulatory T cells (Tregs), cells, innate CVDs diseases. Furthermore, we outline seven immunological principles guide development new ICP-based therapies for CVDs. This timely thorough analysis recent advancements challenges provide insights into role CVDs, Tregs, will support novel therapeutics strategies these

Язык: Английский

Процитировано

1

Perspective: Pathological transdifferentiation—a novel therapeutic target for cardiovascular diseases and chronic inflammation DOI Creative Commons

William Y. Yang,

Melissa Mahgoub,

Fatma Saaoud

и другие.

Frontiers in Cardiovascular Medicine, Год журнала: 2024, Номер 11

Опубликована: Ноя. 26, 2024

Pathological transdifferentiation, where differentiated cells aberrantly transform into other cell types that exacerbate disease rather than promote healing, represents a novel and significant concept. This perspective discusses its role potential targeting in cardiovascular diseases chronic inflammation. Current therapies mainly focus on mitigating early inflammatory response through proinflammatory cytokines pathways targeting, including corticosteroids, TNF-α inhibitors, IL-1β monoclonal antibodies blockers, IL-6 nonsteroidal anti-inflammatory drugs (NSAIDs), along with modulating innate immune memory (trained immunity). However, these approaches often fail to address long-term tissue damage functional regeneration. For instance, fibroblasts can transdifferentiate myofibroblasts cardiac fibrosis, endothelial may undergo mesenchymal transition (EndMT) vascular remodeling, resulting fibrosis impaired function. Targeting pathological transdifferentiation promising therapeutic avenue by focusing key signaling drive aberrant cellular phenotypic transcriptomic transitions. approach seeks inhibit or modulate plasticity effective regeneration prevent fibrosis. Such strategies have the inflammation, death, damage, providing more comprehensive sustainable treatment solution. Future research should understanding mechanisms behind identifying relevant biomarkers master regulators, developing preclinical clinical trials. Integrating new existing treatments could enhance efficacy improve patient outcomes. Highlighting as target paradigms, leading better management recovery of tissues

Язык: Английский

Процитировано

0