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<p>Bone marrow-derived mesenchymal stem cells (BM-MSCs) have demonstrated significant potential owing to their strong immunomodulatory, anti-inflammatory, and regenerative properties. This review explores the antifibrotic effects of BM-MSCs, focusing on their underlying mechanisms, preclinical evidence, and progress in clinical trials. BM-MSCs moderate fibrosis through immune modulation, regulation of myofibroblast differentiation, and stimulation of matrix metalloproteinase (MMP)-mediated degradation of the extracellular matrix (ECM). In pulmonary fibrosis animal models, BM-MSCs reduced TGF-β1 activation and α-SMA and improved lung histology under experimental conditions; some studies included corticosteroid-treated comparators. Additionally, BM-MSCs inhibited the activation of hepatic stellate cells and promoted the polarization of macrophages to an M2 anti-inflammatory phenotype in liver fibrosis. Genetically modified bone marrow-derived mesenchymal stem cells (GM BM-MSCs), such as those transfected with miRNA or overexpressing IL-10, have demonstrated enhanced efficacy in ameliorating myocardial and renal fibrosis through increased homing, paracrine functions, and the inhibition of fibrosis-promoting genes. Early clinical trials of idiopathic pulmonary fibrosis and cirrhotic conditions have indicated their feasibility, safety, and potential efficacy. BM-MSC-derived extracellular vesicles (EVs) provide cell-free therapeutic alternatives with comparable benefits to those of BM-MSCs. Overall, this review provides a comprehensive mechanistic overview of the antifibrotic potential of BM-MSCs, highlighting their translational relevance across organ systems and their promise in regenerative medicine.</p>

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Regenerative Engineering of Fibrotic Diseases: Mechanistic and Clinical Advances with Bone Marrow Mesenchymal Stem Cells

  • 期刊论文

  • 发表日期：

    2025年11月13日

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  • Neeraj Kumar Fuloria,
  • Shivkanya Fuloria,
  • Mahendran Sekar,
  • Omji Porwal,
  • Mohammed Tahir Ansari,
  • Anupam Biswas,
  • Kamal Narain,
  • Sangita Biswas,
  • Sumita Bhatia,
  • Mogana Das Murtey

摘要

Bone marrow-derived mesenchymal stem cells (BM-MSCs) have demonstrated significant potential owing to their strong immunomodulatory, anti-inflammatory, and regenerative properties. This review explores the antifibrotic effects of BM-MSCs, focusing on their underlying mechanisms, preclinical evidence, and progress in clinical trials. BM-MSCs moderate fibrosis through immune modulation, regulation of myofibroblast differentiation, and stimulation of matrix metalloproteinase (MMP)-mediated degradation of the extracellular matrix (ECM). In pulmonary fibrosis animal models, BM-MSCs reduced TGF-β1 activation and α-SMA and improved lung histology under experimental conditions; some studies included corticosteroid-treated comparators. Additionally, BM-MSCs inhibited the activation of hepatic stellate cells and promoted the polarization of macrophages to an M2 anti-inflammatory phenotype in liver fibrosis. Genetically modified bone marrow-derived mesenchymal stem cells (GM BM-MSCs), such as those transfected with miRNA or overexpressing IL-10, have demonstrated enhanced efficacy in ameliorating myocardial and renal fibrosis through increased homing, paracrine functions, and the inhibition of fibrosis-promoting genes. Early clinical trials of idiopathic pulmonary fibrosis and cirrhotic conditions have indicated their feasibility, safety, and potential efficacy. BM-MSC-derived extracellular vesicles (EVs) provide cell-free therapeutic alternatives with comparable benefits to those of BM-MSCs. Overall, this review provides a comprehensive mechanistic overview of the antifibrotic potential of BM-MSCs, highlighting their translational relevance across organ systems and their promise in regenerative medicine.