Fouad Hajjar

Mr. Fouad Hajjar


Research Focus & Metrics

Academic Career Length

3Years (2024-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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26 December 2024 in Biomedicines
Verified
Journal Article
Open access
PDF file
John DawiJohn Dawi
John Dawi
YMYura Misakyan
Yura Misakyan
SAStephen Affa
Stephen Affa
SKSamuel Kades
Samuel Kades
ANAnanya Narasimhan
Ananya Narasimhan
Vishwanath VenketaramanVishwanath Venketaraman
Vishwanath Venketaraman
Type 2 diabetes mellitus (T2DM) is significantly associated with oxidative stress, resulting from the imbalance between reactive oxygen species (ROS) production and antioxidant defenses. This imbalance contributes to insulin resistance, β-cell dysfunction, and complications in organs like the vasculature and nervous system. Glutathione (GSH), a major antioxidant, is crucial for neutralizing ROS, but GSH levels are notably low in T2DM, exacerbating oxidative stress and inflammation. Elevated interleukin-6 (IL-6) levels further intensify inflammation and oxidative stress, disrupting insulin signaling and worsening complications such as nephropathy, retinopathy, and neuropathy. While lifestyle modifications and antioxidant supplementation are current approaches for managing oxidative stress, their effectiveness in preventing complications remains under study. Recent investigations suggest that GSH and Vitamin D3 supplementation may offer dual-action benefits, as Vitamin D3 not only has anti-inflammatory properties but also promotes GSH synthesis. This dual action helps mitigate both oxidative stress and inflammation, addressing key pathological features of T2DM. This review highlights the complex interactions between oxidative stress, GSH insufficiency, and IL-6, and emphasizes the potential of targeted therapies to improve the management and outcomes of T2DM.

17 July 2025 in Biomolecules
Verified
Journal Article
Open access
PDF file
NYNickolas Yedgarian
Nickolas Yedgarian
JAJacqueline Agopian
Jacqueline Agopian
BFBrandon Flaig
Brandon Flaig
Fouad HajjarFouad Hajjar
Fouad Hajjar
AKArshavir Karapetyan
Arshavir Karapetyan
Vishwanath VenketaramanVishwanath Venketaraman
Vishwanath Venketaraman
Mycobacterium tuberculosis—an acid-fast staining bacterium—is a serious global health challenge that can have both short-term and long-term complications. Although the immune response helps trap the infection, it can also cause necrosis and calcification, leading to lung tissue damage. Calcification is a known outcome of chronic granuloma evolution in TB. Multiple pathways contribute to fibrosis and calcification; some examples are IL-1β, TGF-β, and TNF-α. Current antifibrotic drugs, such as nintedanib and pirfenidone, are effective but may increase the risk of latent tuberculosis reactivation in certain patients. Experimental therapies such as artemisinin derivatives have shown promise in preclinical TB fibrosis models, while cell-based therapies like bone marrow-derived mononuclear cells are also under early investigation for dual antifibrotic and immunomodulatory effects. This literature review will explore recent studies on the pathogenesis of M. tuberculosis, the mechanisms underlying calcification in granuloma formation, and subsequent complications of the disease process.