The DOI matches its Crossref record; 118 of the 118 references it cites were found in a registry or an index.
Mechanistic Insights into the Oxidized Low-Density Lipoprotein-Induced Atherosclerosis
Open accessAbstract
Dyslipidaemia has a prominent role in the onset of notorious atherosclerosis, a disease of medium to large arteries. Atherosclerosis is the prime root of cardiovascular events contributing to the most considerable number of morbidity and mortality worldwide. Factors like cellular senescence, genetics, clonal haematopoiesis, sedentary lifestyle-induced obesity, or diabetes mellitus upsurge the tendency of atherosclerosis and are foremost pioneers to definitive transience. Accumulation of oxidized low-density lipoproteins (Ox-LDLs) in the tunica intima triggers the onset of this disease. In the later period of progression, the build-up plaques rupture ensuing thrombosis (completely blocking the blood flow), causing myocardial infarction, stroke, and heart attack, all of which are common atherosclerotic cardiovascular events today. The underlying mechanism is very well elucidated in literature but the therapeutic measures remains to be unleashed. Researchers tussle to demonstrate a clear understanding of treating mechanisms. A century of research suggests that lowering LDL, statin-mediated treatment, HDL, and lipid-profile management should be of prime interest to retard atherosclerosis-induced deaths. We shall brief the Ox-LDL-induced atherogenic mechanism and the treating measures in line to impede the development and progression of atherosclerosis.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Inflammation and Atherosclerosis
Libby, P., Ridker, P. M., & Maseri, A. (2002) · Circulation · doi:10.1161/hc0902.104353 · Cited by 7,724
Regulation of Ferroptotic Cancer Cell Death by GPX4
Yang, W. S., SriRamaratnam, R., Welsch, M. E., Shimada, K., Skouta, R., Viswanathan, V. S., Cheah, J. H., Clemons, P. A., Shamji, A. F., Clish, C. B., et al. (2014) · Cell · doi:10.1016/j.cell.2013.12.010 · Cited by 7,713
Galluzzi, L., Vitale, I., Aaronson, S. A., Abrams, J. M., Adam, D., Agostinis, P., Alnemri, E. S., Altucci, L., Amelio, I., Andrews, D. W., et al. (2018) · Cell Death & Differentiation · doi:10.1038/s41418-017-0012-4 · Cited by 6,680
The Pathogenesis of Atherosclerosis — An Update
Ross, R. (1986) · New England Journal of Medicine · doi:10.1056/nejm198602203140806 · Cited by 4,877
(1994) · New England Journal of Medicine · doi:10.1056/nejm199404143301501 · Cited by 4,737
ROS as signalling molecules: Mechanisms that generate specificity in ROS homeostasis
D'Autréaux, B., & Toledano, M. B. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2256 · Cited by 3,642
Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease
Omenn, G. S., Goodman, G. E., Thornquist, M. D., Balmes, J., Cullen, M. R., Glass, A., Keogh, J. P., Meyskens, F. L., Valanis, B., Williams, J. H., et al. (1996) · New England Journal of Medicine · doi:10.1056/nejm199605023341802 · Cited by 3,638
Sies, H., Berndt, C., & Jones, D. P. (2017) · Annual Review of Biochemistry · doi:10.1146/annurev-biochem-061516-045037 · Cited by 3,520
Libby, P., Buring, J. E., Badimon, L., Hansson, G. K., Deanfield, J., Bittencourt, M. S., Tokgözoğlu, L., & Lewis, E. F. (2019) · Nature Reviews Disease Primers · doi:10.1038/s41572-019-0106-z · Cited by 3,211
Glass, C. K., & Witztum, J. L. (2001) · Cell · doi:10.1016/s0092-8674(01)00238-0 · Cited by 3,051
Research works printed but not linked: 13
- 10.1007/BF00878570 · doi:10.1007/bf00878570
- 10.1016/B978-0-12-386454-3.00327-4 · doi:10.1016/b978-0-12-386454-3.00327-4
- 2013, Lipid Peroxidation: Chemical Mechanism, 13
- 2005, Vascular Health and Risk Management, 1, 183
- 2002, Journal of Cardiac Failure, 2
- 10.1016/j.mpmed.2018.06.010 · doi:10.1016/j.mpmed.2018.06.010
- 2009, Hellenic Journal of Cardiology, 1, 402
- 10.1093/ajcn/54.6.1113sa · doi:10.1093/ajcn/54.6.1113sa
- 10.1146/annurev.nutr.16.1.51 · doi:10.1146/annurev.nutr.16.1.51
- 10.1590/s1984-82502012000100004 · doi:10.1590/s1984-82502012000100004
- 10.1002/ejlt.201200162 · doi:10.1002/ejlt.201200162
- 10.1089/ars.2014.5998 · doi:10.1089/ars.2014.5998
- 10.1016/j.freeradbiomed.2019.09.034.IF-6.4 · doi:10.1016/j.freeradbiomed.2019.09.034.if-6.4
Cited by
Das, D., Shruthi, N. R., Banerjee, A., Jothimani, G., Duttaroy, A. K., & Pathak, S. (2023) · Frontiers in Nutrition · doi:10.3389/fnut.2023.1221438 · Cited by 90
“Increased risk of CVD insulin resistance, and impaired endothelial function are all associated with this condition (180).”
BackgroundThe ABCA1-efferocytosis axis: A new strategy to protect against atherosclerosis
Chen, W., Li, L., Wang, J., Zhang, R., Zhang, T., Wu, Y., Wang, S., & Xing, D. (2021) · Clinica Chimica Acta · doi:10.1016/j.cca.2021.02.025 · Cited by 84
Amirkhizi, F., Taghizadeh, M., Hamedi-Shahraki, S., & Asghari, S. (2025) · Nutrition & Metabolism · doi:10.1186/s12986-025-00932-1 · Cited by 3
“It is considered more atherogenic and inflammatory compared to the native LDL, and is believed to play a significant role in the development of atherosclerosis [60, 61].”
Metadata
- Authors
- Khatana, C., Saini, N. K., Chakrabarti, S., Saini, V., Sharma, A., Saini, R. V., & Saini, A. K.
- Venue
- Oxidative Medicine and Cellular Longevity
- Publisher
- Wiley
- Published
- 2020-09-15
- Volume
- 2020
- Pages
- 1-14
- ISSN
- 1942-0994 (ISSN-L)
- 1942-0900
- OpenAlex
- W3085515718
- Cited by
- 465
- References
- 118
- FWCI
- 12.07
- Type
- journal article
- Language
- en
- Open access
- hybrid
- Funders
- Department of Science and Technology, Government of India (IF180523, SB/S2/RJN-107/2018)
- Ramanuja Fellowship (IF180523, SB/S2/RJN-107/2018)
- Central Research Cell, MMIMSR, M (IF180523, SB/S2/RJN-107/2018)
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Mechanistic Insights into the Oxidized Low-Density Lipoprotein-Induced Atherosclerosis. https://app.cochat.ai/papers/10.1155/2020/5245308
- The paper
- Khatana, C., Saini, N. K., Chakrabarti, S., Saini, V., Sharma, A., Saini, R. V., & Saini, A. K. (2020). Mechanistic Insights into the Oxidized Low-Density Lipoprotein-Induced Atherosclerosis. Oxidative Medicine and Cellular Longevity. https://doi.org/10.1155/2020/5245308
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
