ReviewCells2022
New Insights into the Mechanisms of Chaperon-Mediated Autophagy and Implications for Kidney Diseases.
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Review
- Molecular engineering of lysosome-based degraders unveils a rapidly expanding therapeutic strategy.Autophagy · 2026Review
- HSP90AA1 Facilitates Vascular Calcification in Chronic Kidney Disease Involving Chaperone-Mediated Autophagy.Biomedicines · 2026Article
- Critical Roles and Molecular Mechanisms of Chaperone-Mediated Autophagy in Infections.International journal of molecular sciences · 2026Review
- Chaperone-mediated autophagy ameliorates hyperlipidemia-induced apoptosis in podocytes via attenuating lipid accumulation.Journal of molecular histology · 2026Article
- Autophagy Dysregulation in Crohn's Disease and Colorectal Cancer-An Analysis ofCurrent issues in molecular biology · 2025Article
- Role of Autophagy in Type 2 Diabetes Mellitus: The Metabolic Clash.Journal of cellular and molecular medicine · 2024Review
- Targeted protein degradation: advances in drug discovery and clinical practice.Signal transduction and targeted therapy · 2024Review
- Expression of Autophagy Markers LC3B, LAMP2A, and GRP78 in the Human Kidney during Embryonic, Early Fetal, and Postnatal Development and Their Significance in Diabetic Kidney Disease.International journal of molecular sciences · 2024Article
- Mechanisms and implications of podocyte autophagy in chronic kidney disease.American journal of physiology. Renal physiology · 2024Review
- Review
- The Role of Chaperone-Mediated Autophagy in Tissue Homeostasis and Disease Pathogenesis.Biomedicines · 2024Review
- The role of lysosomes in metabolic and autoimmune diseases.Nature reviews. Nephrology · 2023Review
- The Dual Role of Oxidative-Stress-Induced Autophagy in Cellular Senescence: Comprehension and Therapeutic Approaches.Antioxidants (Basel, Switzerland) · 2023Review
- Article
- Transcriptomic signatures responding to PKM2 activator TEPP-46 in the hyperglycemic human renal proximal epithelial tubular cells.Frontiers in endocrinology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Chaperone-mediated autophagy (CMA) is a separate type of lysosomal proteolysis, characterized by its selectivity of substrate proteins and direct translocation into lysosomes. Recent studies have declared the involvement of CMA in a variety of physiologic and pathologic situations involving the kidney, and it has emerged as a potential target for the treatment of kidney diseases. The role of CMA in kidney diseases is context-dependent and appears reciprocally with macroautophagy. Among the renal resident cells, the proximal tubule exhibits a high basal level of CMA activity, and restoration of CMA alleviates the aging-related tubular alternations. The level of CMA is up-regulated under conditions of oxidative stress, such as in acute kidney injury, while it is declined in chronic kidney disease and aging-related kidney diseases, leading to the accumulation of oxidized substrates. Suppressed CMA leads to the kidney hypertrophy in diabetes mellitus, and the increase of CMA contributes to the progress and chemoresistance in renal cell carcinoma. With the progress on the understanding of the cellular functions and uncovering the clinical scenario, the application of targeting CMA in the treatment of kidney diseases is expected.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.