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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

Intrinsic Inflammatory Signaling in Life and Death of Podocytes

  • Danila E. Bobkov1,2
  • Sofya A. Konopleva1
  • Dmitry A. Osin1
  • Oleg N. Demidov1,2,3
  • Veronika S. Mihailovskaya4
4 affiliations
  1. 1Department of Immunobiology and Biomedicine, Sirius University of Science and Technology, 354340 Sirius, Russia
  2. 2Institute of Cytology, Russian Academy of Sciences, 194064 St. Petersburg, Russia
  3. 3INSERM UMR1231, University of Burgundy, 21078 Dijon, France
  4. 4Institute of Ecology and Genetics of Microorganisms, Ural Branch of the Russian Academy of Sciences, 614081 Perm, Russia
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Abstract

Podocytes are terminally differentiated components of the glomerular filtration barrier whose structural integrity depends on coordinated signaling between the slit diaphragm, actin cytoskeleton, mitochondria, and stress-response machinery. Evidence from cultured podocytes, experimental kidney disease, human tissue, and selected podocyte-specific genetic models indicates that podocytes can execute intrinsic inflammatory responses and, in defined settings, contribute to local inflammatory amplification. This review examines how NF-κB, p38 MAPK, JAK–STAT, cGAS–STING, NLRP3 inflammasome, and Rho-family GTPase signaling interact with cytoskeletal remodeling, mitochondrial dysfunction, senescence, regulated cell death, and podocyte detachment. Particular attention is given to the distinction between podocyte-specific evidence and findings obtained from whole-kidney analyses, global genetic models, or pharmacological interventions. The available evidence supports a context-dependent network in which inflammatory signaling may support adaptation but, when sustained or dysregulated, can contribute to barrier dysfunction and irreversible podocyte loss. We also assess therapeutic strategies targeting inflammatory sensors, kinases, inflammasome components, cytoskeletal regulators, and metabolic stress pathways. Most remain preclinical, emphasizing the need for podocyte-targeted delivery, rigorous cell-specific validation, and human translational studies.

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Cite

BibTeXRIS
BibTeX
@article{bobkov2026intrinsic,
  title = {{Intrinsic Inflammatory Signaling in Life and Death of Podocytes}},
  author = {Danila E. Bobkov and Sofya A. Konopleva and Dmitry A. Osin and Oleg N. Demidov and Veronika S. Mihailovskaya},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = nov,
  doi = {10.3390/ijms27219923},
  url = {https://www.mdpi.com/1422-0067/27/21/9923},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Intrinsic Inflammatory Signaling in Life and Death of Podocytes
AU  - Danila E. Bobkov
AU  - Sofya A. Konopleva
AU  - Dmitry A. Osin
AU  - Oleg N. Demidov
AU  - Veronika S. Mihailovskaya
PY  - 2026
DA  - 2026/11/05
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27219923
UR  - https://www.mdpi.com/1422-0067/27/21/9923
AB  - Podocytes are terminally differentiated components of the glomerular filtration barrier whose structural integrity depends on coordinated signaling between the slit diaphragm, actin cytoskeleton, mitochondria, and stress-response machinery. Evidence from cultured podocytes, experimental kidney disease, human tissue, and selected podocyte-specific genetic models indicates that podocytes can execute intrinsic inflammatory responses and, in defined settings, contribute to local inflammatory amplification. This review examines how NF-κB, p38 MAPK, JAK–STAT, cGAS–STING, NLRP3 inflammasome, and Rho-family GTPase signaling interact with cytoskeletal remodeling, mitochondrial dysfunction, senescence, regulated cell death, and podocyte detachment. Particular attention is given to the distinction between podocyte-specific evidence and findings obtained from whole-kidney analyses, global genetic models, or pharmacological interventions. The available evidence supports a context-dependent network in which inflammatory signaling may support adaptation but, when sustained or dysregulated, can contribute to barrier dysfunction and irreversible podocyte loss. We also assess therapeutic strategies targeting inflammatory sensors, kinases, inflammasome components, cytoskeletal regulators, and metabolic stress pathways. Most remain preclinical, emphasizing the need for podocyte-targeted delivery, rigorous cell-specific validation, and human translational studies.
SN  - 1422-0067
ER  -