Paul D Robbins
Overview
Explore the profile of Paul D Robbins including associated specialties, affiliations and a list of published articles.
Author names and details appear as published. Due to indexing inconsistencies, multiple individuals may share a name, and a single author may have variations. MedLuna displays this data as publicly available, without modification or verification
Snapshot
Snapshot
Articles
254
Citations
21769
Followers
0
Related Specialties
Related Specialties
Top 10 Co-Authors
Top 10 Co-Authors
Published In
Published In
Affiliations
Affiliations
Soon will be listed here.
Recent Articles
11.
Grange C, Papadimitriou E, Dimuccio V, Pastorino C, Molina J, OKelly R, et al.
Mol Ther
. 2024 Sep;
32(11):4158-4159.
PMID: 39293431
No abstract available.
12.
Evans C, Ghivizzani S, Robbins P
J Am Acad Orthop Surg
. 2024 Sep;
32(23):1052-1060.
PMID: 39284030
Osteoarthritis (OA) is a highly prevalent, disabling, incurable, and expensive disease that is difficult to treat nonsurgically. The pharmacokinetics of drug delivery to joints are such that it is not...
13.
Lin J, Sin-Chan P, Napolioni V, Torres G, Mitra J, Zhang Q, et al.
Nat Aging
. 2024 Aug;
4(9):1328.
PMID: 39198704
No abstract available.
14.
Calubag M, Robbins P, Lamming D
Cell Metab
. 2024 Aug;
36(9):1914-1944.
PMID: 39178854
Cellular senescence, a process in which a cell exits the cell cycle in response to stressors, is one of the hallmarks of aging. Senescence and the senescence-associated secretory phenotype (SASP)-a...
15.
Ogrodnik M, Carlos Acosta J, Adams P, dAdda di Fagagna F, Baker D, Bishop C, et al.
Cell
. 2024 Aug;
187(16):4150-4175.
PMID: 39121846
Cellular senescence is a cell fate triggered in response to stress and is characterized by stable cell-cycle arrest and a hypersecretory state. It has diverse biological roles, ranging from tissue...
16.
Mahmud S, Pitcher L, Torbenson E, Robbins P, Zhang L, Dong X
Ageing Res Rev
. 2024 Jul;
99:102403.
PMID: 38964507
Cellular senescence is a cell fate driven by different types of stress, where damaged cells exit from the cell cycle and, in many cases, develop an inflammatory senescence-associated secretory phenotype...
17.
Rajamani G, Stafki S, Daugherty A, Mantyh W, Littel H, Bruels C, et al.
Neurol Clin Pract
. 2024 May;
14(4):e200309.
PMID: 38808024
Background And Objectives: Cockayne syndrome (CS) is an ultra-rare, autosomal recessive, premature aging disorder characterized by impaired growth, neurodevelopmental delays, neurodegeneration, polyneuropathy, and other multiorgan system complications. The anatomic aspects...
18.
Hambright W, Duke V, Goff A, Goff A, Minas L, Kloser H, et al.
Aging Cell
. 2024 May;
23(5):e14113.
PMID: 38708778
Chronic conditions associated with aging have proven difficult to prevent or treat. Senescence is a cell fate defined by loss of proliferative capacity and the development of a pro-inflammatory senescence-associated...
19.
Yousefzadeh M, Huerta Guevara A, Postmus A, Flores R, Sano T, Jurdzinski A, et al.
Aging Biol
. 2023 Dec;
1(1).
PMID: 38124711
Age is the greatest risk factor for the development of type 2 diabetes mellitus (T2DM). Age-related decline in organ function is attributed to the accumulation of stochastic damage, including damage...
20.
Saul D, Jurk D, Doolittle M, Kosinsky R, Monroe D, LeBrasseur N, et al.
bioRxiv
. 2023 Dec;
PMID: 38106149
Senescent cells drive age-related tissue dysfunction via the induction of a chronic senescenceassociated secretory phenotype (SASP). The cyclin-dependent kinase inhibitors p21 and p16 have long served as markers of cellular...