What this means
Autophagy is a fundamental cellular process that maintains homeostasis by degrading and recycling cellular components. As autophagy is essential for metabolizing damaged organelles and toxic substances, it plays a crucial role in both normal physiology and pathological conditions.
A plain-English summary is on its way. Until then, this is the start of the authors' own summary.
- Who it was tested in
- Earlier studies
- Kind of research
- A summary of earlier studies
The science
- Original title
- Harnessing autophagy and its transcriptional regulation in tumorigenesis and neurodegeneration: Potential and existing therapeutic strategies.
- Authors
- Suri P, Daartey AB, Olive Khan DMI et al.
- Journal
- Pharmacological reviews
- Published
- Oct 16, 2026
- Study type
- Review
- PMID
- 42887433 ↗
Abstract
Autophagy is a fundamental cellular process that maintains homeostasis by degrading and recycling cellular components. As autophagy is essential for metabolizing damaged organelles and toxic substances, it plays a crucial role in both normal physiology and pathological conditions. However, autophagy has dual roles in both tumorigenesis and neurodegeneration. In cancer, autophagy can act as a tumor suppressor by clearing damaged components in early stages, but promotes tumor survival and growth in later stages, particularly under stress. In neurodegeneration, impaired autophagy is implicated in the disease progression of conditions such as Alzheimer, Parkinson, and Huntington diseases, in which the failure to clear misfolded proteins and damaged organelles exacerbates disease pathology. This review is organized to cover the molecular machinery and transcriptional regulation of autophagy, its disease-specific subtypes, its dual roles in tumorigenesis and neurodegeneration, and the current pharmacological landscape for therapeutic targeting. Attention is given to pharmacological modulation of autophagy, including senolytic drugs that selectively eliminate senescent cells by exploiting their dependence on antiapoptotic survival pathways, and small-molecule regulators targeting key pathways such as phosphoinositide 3-kinase/Akt serine/threonine kinase/mechanistic target of rapamycin and AMP-activated protein kinase. Depending on the pathological context, these drugs are under development to either inhibit or induce autophagy. Additionally, we address the challenges and limitations in developing effective autophagy-targeting drugs, underscoring the need for further research to identify new compounds that can modulate cellular autophagic flux. SIGNIFICANCE STATEMENT: Autophagy is an important homeostatic mechanism, and its dysregulation contributes to a wide range of diseases, including cancer and neurodegenerative disorders. Therefore, a deeper mechanistic understanding of the regulation of autophagy is crucial for advancing targeted therapies with significant clinical impact.
Suri P, Daartey AB, Olive Khan DMI et al. Harnessing autophagy and its transcriptional regulation in tumorigenesis and neurodegeneration: Potential and existing therapeutic strategies. Pharmacological reviews. 2026. doi:10.1016/j.pharmr.2026.100158. PMID: 42887433. https://pubmed.ncbi.nlm.nih.gov/42887433/
Related research
New fluorescent sensor detects cells aging from cancer and lung drugs
Researchers built a glowing probe that lights up only in certain aged cells. It may help scientists track these cells in living animals, but this is early lab work.
Mixing a senescence-clearing drug with trametinib slowed glioma regrowth in mice
Researchers found a drug combination that cleared aging-like tumour cells in mice and slowed regrowth. This does not show the combination would work the same way in children.
A vaccine-style treatment in mice eased diabetes signs and aged cell markers
Mice given a treatment aimed at a virus-like gene showed less weight gain and better blood sugar control. This study was in mice and cells, so it does not show the same would happen in people.
Aging cells that support stem cells may disrupt them through chemical signals
This is a review that pulls together older and newer studies. It proposes a model, but it does not show that the model is true.
Cx43 protein may boost breast cancer drug response in lab tests
Researchers studied a protein called Cx43 that helps cells talk to each other. They found it may help a breast cancer drug slow tumor growth. This early work is not yet checked by other scientists, so it does not show this would help people.
Ginseng compound Rb1 eased signs of aging in the uterus in lab tests
Researchers found that Rb1 reduced aging signs in uterus lining cells and mouse uteruses. This does not show Rb1 helps aging uteruses in people.
See all research on Senolytics →
